Review

Quorum sensing in Acinetobacter: with special emphasis on antibiotic resistance, biofilm formation and quorum quenching

  • Acinetobacter is an important nosocomial, opportunistic human pathogen that is gradually gaining more attention as a major health threat worldwide. Quorum sensing (QS) is a cell-cell communication system in which specific signaling molecules called autoinducers accumulate in the medium as the population density grows and control various physiological processes including production of virulence factors, biofilm and development of antibiotic resistance. The complex QS machinery in Acinetobacter is mediated by a two-component system which is homologous to the typical LuxI/LuxR system found in Gram-negative bacteria. This cell signaling system comprises of a sensor protein that functions as autoinducer synthase and a receptor protein which binds to the signal molecules, acyl homoserine lactones inducing a cascade of reactions. Lately, disruption of QS has emerged as an anti-virulence strategy with great therapeutic potential. Here, we depict the current understanding of the existing QS network in Acinetobacter and describe important anti-virulent strategies developed in order to effectively tackle this pathogen. In addition, the prospects of quorum quenching to control Acinetobacter infections is also been discussed.

    Citation: Bindu Subhadra, Man Hwan Oh, Chul Hee Choi. Quorum sensing in Acinetobacter: with special emphasis on antibiotic resistance, biofilm formation and quorum quenching[J]. AIMS Microbiology, 2016, 2(1): 27-41. doi: 10.3934/microbiol.2016.1.27

    Related Papers:

    [1] Wen Huang, Leiye Xu, Shengnan Xu . Ergodic measures of intermediate entropy for affine transformations of nilmanifolds. Electronic Research Archive, 2021, 29(4): 2819-2827. doi: 10.3934/era.2021015
    [2] Hanan H. Sakr, Mohamed S. Mohamed . On residual cumulative generalized exponential entropy and its application in human health. Electronic Research Archive, 2025, 33(3): 1633-1666. doi: 10.3934/era.2025077
    [3] Mingtao Cui, Wang Li, Guang Li, Xiaobo Wang . The asymptotic concentration approach combined with isogeometric analysis for topology optimization of two-dimensional linear elasticity structures. Electronic Research Archive, 2023, 31(7): 3848-3878. doi: 10.3934/era.2023196
    [4] Julian Gerstenberg, Ralph Neininger, Denis Spiegel . On solutions of the distributional Bellman equation. Electronic Research Archive, 2023, 31(8): 4459-4483. doi: 10.3934/era.2023228
    [5] Natália Bebiano, João da Providência, Wei-Ru Xu . Approximations for the von Neumann and Rényi entropies of graphs with circulant type Laplacians. Electronic Research Archive, 2022, 30(5): 1864-1880. doi: 10.3934/era.2022094
    [6] Xiang Xu . Recent analytic development of the dynamic $ Q $-tensor theory for nematic liquid crystals. Electronic Research Archive, 2022, 30(6): 2220-2246. doi: 10.3934/era.2022113
    [7] Agustín Moreno Cañadas, Pedro Fernando Fernández Espinosa, José Gregorio Rodríguez-Nieto, Odette M Mendez, Ricardo Hugo Arteaga-Bastidas . Extended Brauer analysis of some Dynkin and Euclidean diagrams. Electronic Research Archive, 2024, 32(10): 5752-5782. doi: 10.3934/era.2024266
    [8] Yu Chen, Qingyang Meng, Zhibo Liu, Zhuanzhe Zhao, Yongming Liu, Zhijian Tu, Haoran Zhu . Research on filtering method of rolling bearing vibration signal based on improved Morlet wavelet. Electronic Research Archive, 2024, 32(1): 241-262. doi: 10.3934/era.2024012
    [9] Zhenhua Wang, Jinlong Yang, Chuansheng Dong, Xi Zhang, Congqin Yi, Jiuhu Sun . SSMM-DS: A semantic segmentation model for mangroves based on Deeplabv3+ with swin transformer. Electronic Research Archive, 2024, 32(10): 5615-5632. doi: 10.3934/era.2024260
    [10] Suhua Wang, Zhen Huang, Bingjie Zhang, Xiantao Heng, Yeyi Jiang, Xiaoxin Sun . Plot-aware transformer for recommender systems. Electronic Research Archive, 2023, 31(6): 3169-3186. doi: 10.3934/era.2023160
  • Acinetobacter is an important nosocomial, opportunistic human pathogen that is gradually gaining more attention as a major health threat worldwide. Quorum sensing (QS) is a cell-cell communication system in which specific signaling molecules called autoinducers accumulate in the medium as the population density grows and control various physiological processes including production of virulence factors, biofilm and development of antibiotic resistance. The complex QS machinery in Acinetobacter is mediated by a two-component system which is homologous to the typical LuxI/LuxR system found in Gram-negative bacteria. This cell signaling system comprises of a sensor protein that functions as autoinducer synthase and a receptor protein which binds to the signal molecules, acyl homoserine lactones inducing a cascade of reactions. Lately, disruption of QS has emerged as an anti-virulence strategy with great therapeutic potential. Here, we depict the current understanding of the existing QS network in Acinetobacter and describe important anti-virulent strategies developed in order to effectively tackle this pathogen. In addition, the prospects of quorum quenching to control Acinetobacter infections is also been discussed.


    Throughout this paper, by a topological dynamical system $ (X,T) $ (TDS for short) we mean a compact metric space $ (X,d) $ with a homeomorphism map $ T $ from $ X $ onto itself, where $ d $ refers to the metric on $ X $. By a measure preserving system (MPS for short) we mean a quadruple $ (X,\mathcal{X},\mu,T) $, where $ (X,\mathcal{X},\mu) $ is a Borel probability space and $ T, T^{-1}:X\rightarrow X $ are both measurable and measure preserving, i.e. $ T^{-1}\mathcal{X} = \mathcal{X} = T\mathcal{X} $ and $ \mu(A) = \mu(T^{-1}A) $ for each $ A\in \mathcal{X} $.

    Given a TDS $ (X,T) $, let $ \mathcal{M}(X,T) $ be the set of all $ T $-invariant Borel probability measures of $ X $. In weak$ ^* $-topology, $ \mathcal{M}(X,T) $ is a compact convex space. By Krylov-Bogolioubov Theorem $ \mathcal{M}(X,T)\neq \emptyset $. For each $ \mu\in \mathcal{M}(X,T) $, $ (X,\mathcal{B}_X,T,\mu) $ can be viewed as a MPS, where $ \mathcal{B}_X $ is the Borel $ \sigma $-algebra of $ X $. Let $ \mathcal{M}^e(X,T) $ be the space of all ergodic measures of $ (X, T) $. Then $ \mathcal{M}^e(X,T) $ is the set of extreme points of $ \mathcal{M}(X,T) $.

    Define

    $ \mathcal{E}(T) = \{h_\mu(T):\mu\in\mathcal{M}^e(X,T)\} $

    where $ h_\mu(T) $ denotes the measure-theoretic entropy of the measure preserving system $ (X,\mathcal{B}_X,T,\mu) $. By the variational principle of entropy $ \sup \mathcal{E}(T) = h_{top}(T) $, where $ h_{top}(T) $ is the topological entropy of $ (X,T) $. The extreme case is that $ \mathcal{M}^{e}(X,T) $ consists of only one member, that is, $ (X,T) $ is uniquely ergodic. When $ (X,T) $ is uniquely ergodic, $ \mathcal{E}(T) = \{h_{top}(T)\} $.

    It is interesting to consider the case when $ \mathcal{E}(T) $ is big. As a direct corollary of [7,Theorem 11], Katok showed that

    $ [0,htop(f))E(f)
    $
    (1.1)

    for any $ C^{1+\alpha} $ diffeomorphism $ f $ on a two-dimensional surface, based on the fact that every ergodic measure of positive metric entropy is hyperbolic. Katok conjectured that (1.1) holds for any smooth system.

    Conjecture 1.1 (Katok). Let $ f $ be a $ C^r $ ($ r>1 $) diffeomorphism on a smooth compact manifold $ M $, then (1.1) holds, i.e. for every $ a\in [0,h_{top}(f)) $, there is $ \mu_a\in \mathcal{M}^e(M,f) $ such that $ h_{\mu_a}(f) = a $.

    We need to point out that Katok's conjecture implies that any positive entropy smooth system is not uniquely ergodic, though whether or not a smooth diffeomorphism of positive topological entropy can be uniquely ergodic is still in question (see [5] for Herman's example: positive entropy minimal $ C^\infty $-smooth diffeomorphisms). In [13,14], Quas and Soo showed that if a topological dynamical system satisfies asymptotic entropy expansiveness, almost weak specification property and small boundary property, then it is universal, which implies the conclusion of Katok's conjeture. Recently, Burguet [2], Chandgotia and Meyerovitch [4], extended the result of Quas and Soo to request only the almost weak specification property.

    In this paper, we study intermediate entropy for affine transformations of nilmanifolds. Throughout this paper, by a nilmanifold $ G/\Gamma $ we mean that $ G $ is a connected, simply connected nilpotent Lie group, and $ \Gamma $ is a cocompact discrete subgroup of $ G $. A homeomorphism $ \tau $ of $ G/\Gamma $ is an affine transformation if there exist a $ \Gamma $-invariant automorphism $ A $ of $ G $ and a fixed element $ g_0\in G $ such that $ \tau(g\Gamma) = g_0A(g)\Gamma $ for each $ g\in G $. Our main result is the following.

    Theorem 1.2. Let $ G/\Gamma $ be a nilmanifold and $ \tau $ be an affine transformation of $ G/\Gamma $. If $ (G/\Gamma,\tau) $ has a periodic point, then $ \mathcal{E}(\tau) = [0, h_{top}(\tau)] $.

    Following Lind [11], we say that an affine transformation of a nilmanifold is quasi-hyperbolic if its associated matrix has no eigenvalue 1. As an application of Theorem 1.2, one has the following.

    Theorem 1.3. Let $ G/\Gamma $ be a nilmanifold and $ \tau $ be an affine transformation of $ G/\Gamma $. If $ \tau $ is quasi-hyperbolic, then $ \mathcal{E}(\tau) = [0, h_{top}(\tau)] $.

    The paper is organized as follows. In Section 2, we introduce some notions. In Section 3, we prove Theorem 1.2 and Theorem 1.3.

    In this section, we recall some notions of entropy, nilmanifold and upper semicontinuity of entropy map.

    We summarize some basic concepts and useful properties related to topological entropy and measure-theoretic entropy here.

    Let $ (X,T) $ be a TDS. A cover of $ X $ is a family of subsets of $ X $, whose union is X. A partition of $ X $ is a cover of X whose elements are pairwise disjoint. Given two covers $ \mathcal{U},\mathcal{V} $ of $ X $, set $ \mathcal{U}\vee \mathcal{V} = \{ U\cap V:U\in \mathcal{U},V\in \mathcal{V}\} $ and $ T^{-i}\mathcal{U} = \{T^{-i}U: U\in \mathcal{U}\} $ for $ i\in \mathbb{Z}_+ $. Denote by $ {N}(\mathcal{U}) $ the minimal cardinality among all cardinalities of subcovers of $ \mathcal{U} $.

    Definition 2.1. Let $ (X,T) $ be a TDS and $ \mathcal{U} $ be a finite open cover of $ X $. The topological entropy of $ \mathcal{U} $ is defined by

    $ h_{top}(T,\mathcal{U}) = \lim\limits_{n\rightarrow +\infty}\frac{1}{n}\log {N}(\bigvee_{i = 0}^{n-1}T^{-i}\mathcal{U}), $

    where $ \{\log {N}(\bigvee_{i = 0}^{n-1}T^{-i}\mathcal{U})\}_{n = 1}^\infty $ is a sub-additive sequence and hence $ h_{top}(T,\mathcal{U}) $ is well defined. The topological entropy of $ (X,T) $ is

    $ h_{top}(T) = \sup\limits_{\mathcal{U}} h_{top}(T,\mathcal{U}), $

    where supremum is taken over all finite open covers of $ X $.

    A subset $ E $ of $ X $ is an $ (n, \epsilon) $-separated set with respect to $ T $ provided that for any distinct $ x,y\in E $ there is $ 0\le j<n $ such that $ d(T^jx, T^jy)\ge\epsilon $. Let $ K $ be a compact subset of $ X $. Let $ s_n^{(T)}(\epsilon, K) $ be the largest cardinality of any subset $ E $ of $ K $ which is an $ (n, \epsilon) $-separated set. Then the Bowen's topological entropy of $ K $ with respect to $ T $ [1] is defined by

    $ h_d(T,K) = \lim\limits_{\epsilon\to0}\limsup\limits_{n\to\infty}\frac{\log s^{(T)}_n(\epsilon,K)}{n}. $

    Let $ Z $ be a non-empty subset of $ X $. The Bowen's topological entropy of $ Z $ with respect to $ T $ is defined by

    $ h_d(T,Z) = \sup\limits_{K\subset Z\atop K\text{ is compact}}h_d(T,K). $

    And the Bowen's topological entropy of a TDS $ (X,T) $ is defined by $ h_d(T) = h_d(T,X) $ which happens to coincide with $ h_{top}(T) $.

    Next we define measure-theoretic entropy. Let $ (X,\mathcal{X},\mu,T) $ be a MPS and $ \mathcal{P}_X $ be the set of finite measurable partitions of $ X $. Suppose $ \xi\in \mathcal{P}_X $. The entropy of $ \xi $ is defined by

    $ h_{\mu}(T,\xi) = \lim\limits_{n\rightarrow +\infty} \frac{1}{n} H_\mu(\bigvee_{i = 0}^{n-1}T^{-i}{\xi}), $

    where $ H_\mu(\bigvee_{i = 0}^{n-1}T^{-i}{\xi}) = -\sum _{A\in \bigvee_{i = 0}^{n-1}T^{-i}{\xi}} \mu (A)\log \mu(A) $ and $ \{H_\mu(\bigvee_{i = 0}^{n-1}T^{-i}{\xi})\}_{n = 1}^\infty $ is a sub-additive sequence. The entropy of $ (X,\mathcal{X},T,\mu) $ is defined by

    $ h_{\mu}(T) = \sup\limits_{\xi\in \mathcal{P}_X} h_\mu(T,\xi). $

    The basic relationship between topological entropy and measure-theoretic entropy is given by the variational principle [12].

    Theorem 2.2 (The variational principle). Let $ (X, T ) $ be a TDS. Then

    $ h_{top}(T) = \sup\{h_\mu(T): \mu\in \mathcal{M}(X,T)\} = \sup\{h_\mu(T): \mu\in \mathcal{M}^e(X,T)\}. $

    A factor map $ \pi: (X,T)\rightarrow (Y,S) $ between the TDS $ (X,T) $ and $ (Y,S) $ is a continuous onto map with $ \pi\circ T = S\circ \pi $; we say that $ (Y,S) $ is a factor of $ (X,T) $ and that $ (X,T) $ is an extension of $ (Y,S) $. The systems are said to be conjugate if $ \pi $ is bijective. In [8], Ledrappier and Walters showed that if $ \pi: (X,T)\rightarrow (Y,S) $ is a factor map and $ \nu\in\mathcal{M}(Y,S) $, then

    $ supμM(X,T)π(μ)=νhμ(T)=hν(S)+Yhd(T,π1(y))dν(y)
    $
    (2.1)

    where $ \pi(\mu)(B) = \mu(\pi^{-1}(B)) $ for $ B\in\mathcal{B}_Y $.

    Let $ G $ be a compact metric group and $ \tau:G\to G $ be a continuous surjective map. Let $ \pi:(X,T)\to (Y,S) $ be a factor map. We say that $ \pi $ is a $ (G,\tau) $-extension, if there exists a continuous map $ P: X\times G\to X $ (we write $ P(x, g) = xg $) such that:

    $ (1) $ $ \pi^{-1}(\pi(x)) = xG $ for $ x\in X $,

    $ (2) $ For any $ x\in X,g_1,g_2\in G $, $ xg_1 = xg_2 $ if and only if $ g_1 = g_2 $,

    $ (3) T(xg) = T(x)\tau( g) $ for $ x\in X $ and $ g\in G $.

    The following is from [1,Theorem 19].

    Theorem 2.3. Let $ \pi:(X,T)\to (Y,S) $ be a factor map. If $ \pi $ is a $ (G,\tau) $-extension, then $ h_{top}(T) = h_{top}(S)+h_{top}(\tau) $.

    Remark 2.4. (1) In the above situation, Bowen shows that

    $ hd(T,π1(y))=htop(τ) for any yY,
    $
    (2.2)

    where $ d $ is the metric on $ X $. This fact is proved in the proof of [1,Theorem 19]. In fact, (2.2) holds in the more general situation of actions of amenable groups. This fact is given explicitly as Lemma 6.12 in the paper [10].

    (2) If $ G $ is a Lie group, $ H $ and $ N $ are cocompact closed subgroups of $ G $ such that $ N $ is a normal subgroup of $ H $, then $ G/N $ and $ G/H $ are compact metric spaces and $ H/N $ is a compact metric group. Given further $ g_0 \in G $ and an automorphism $ A $ of $ G $ preserving $ H $ and $ N $, one has the affine maps $ T : G/N \to G/N $ given by $ T(gN) = g_0A(g)N $, and $ S:G/H \to G/H $ given by $ S(gH) = g_0A(g)H $, and the automorphism $ \tau $ of $ H/N $ given by $ \tau (hN) = A(h)N $. Then there is a map $ \pi: G/N\to G/H $ given by $ \pi(gN) = gH $ for $ g\in G $, and a map $ P : G/N \times H/N \to G/N $ given by $ P(gN, hN) = ghN $ for $ g,h\in G $. These maps satisfy the conditions $ (1)- (3) $ in the definition of $ (H/N,\tau) $-extension for the factor map $ \pi:(G/N,T)\to (G/H,S) $. That is, $ (G/N, T) $ is an $ (H/N, \tau ) $-extension of $ (G/H, S) $. Hence one has by (2.2) that

    $ hd(T,π1(y))=htop(τ) for any yG/H,
    $
    (2.3)

    where $ d $ is the metric on $ G/N $.

    Given a TDS $ (X,T) $, the entropy map of $ (X,T) $ is the map $ \mu\mapsto h_\mu(T) $ which is defined on $ \mathcal{M}(X,T) $ and has value in $ [0,\infty] $. For any invariant measure $ \mu $ on $ X $, there is a unique Borel probability measure $ \rho $ on $ \mathcal{M}(X,T) $ with $ \rho(\mathcal{M}^e(X,T)) = 1 $ such that

    $ \int_{\mathcal{M}^e(X,T)}\int_X f(x)dm(x)d\rho(m) = \int_Xf(x)d\mu(x)\text{ for all }f\in C(X). $

    We write $ \mu = \int_{\mathcal{M}^e(X,T)}md\rho(m) $ and call it the ergodic decomposition of $ \mu $. The following is standard.

    Theorem 2.5. Let $ (X,T) $ be a TDS. If $ \mu\in\mathcal{M}(X,T) $ and $ \mu = \int_{\mathcal{M}^e(X,T)}md\rho(m) $ is the ergodic decomposition of $ \mu $. Then

    $ h_\mu(T) = \int_{\mathcal{M}^e(X,T)}h_m(T)d\rho(m). $

    We say that the entropy map of $ (X,T) $ is upper semicontinuous if for $ \mu_n,\mu\in\mathcal{M}(X,T) $

    $ \lim\limits_{n\to\infty}\mu_n = \mu \text{ implies }\limsup\limits_{n\to\infty}h_{\mu_n}(T)\le h_{\mu}(T). $

    We say that a TDS $ (X,T) $ satisfies asymptotic entropy expansiveness if

    $ \lim \limits_{\delta\rightarrow 0} \sup\limits_{x\in X} h_{d}(T,\Gamma_\delta(x)) = 0. $

    Here for each $ \delta>0 $,

    $ \Gamma_\delta(x) : = \{y \in X: d( T^jx,T^jy) < \delta \text{ for all }j\ge 0\}. $

    The result of Misiurewicz [12,Corollary 4.1] gives a sufficient condition for upper semicontinuity of the entropy map.

    Theorem 2.6. Let $ (X,T) $ be a TDS. If $ (X,T) $ satisfies asymptotic entropy expansiveness. Then the entropy map of $ (X,T) $ is upper semicontinuous.

    The result of Buzzi [3] gives a sufficient condition for asymptotic entropy expansiveness.

    Theorem 2.7. Let $ f $ be a $ C^\infty $ diffeomorphism on a smooth compact manifold $ M $, then $ (M,f) $ satisfies asymptotic entropy expansiveness. Especially, the entropy map of $ (M,f) $ is upper semicontinuous.

    In this section, we prove our main results. In the first subsection, we prove that Katok's conjecture holds for affine transformations of torus. In the second subsection, we show some properties of metrics on nilmanifolds. In the last subsection, we prove Theorem 1.2 and Theorem 1.3.

    We say that a topological dynamical system $ (Y, S) $ is universal if for every invertible non-atomic ergodic measure preserving system $ (X,\mathcal{X}, \mu, T) $ with measure-theoretic entropy strictly less than the topological entropy of $ S $ there exists $ \nu\in \mathcal{M}^e(Y,S) $ such that $ (X,\mathcal{X}, \mu, T) $ is isomorphic to $ (Y,\mathcal{B}_Y,\nu, S) $. In [14], Quas and Soo show that toral automorphisms are universal, which implies the conclusion of Katok's conjeture. By using Quas and Soo's result, we have the following.

    Theorem 3.1. Let $ m\in\mathbb{N} $, $ \mathbb{T}^m = \mathbb{R}^m/\mathbb{Z}^m $ and $ \tau $ be an affine transformation of $ \mathbb{T}^m $. Then $ \mathcal{E}(\tau) = [0, h_{top}(\tau)] $.

    Proof. We think of $ \mathbb{T}^m $ as a group. Then there exist an element $ b\in\mathbb{T}^m $ and a toral automorphism $ A $ of $ \mathbb{T}^m $ such that

    $ \tau(x) = A(x)+b\text{ for each }x\in \mathbb{T}^m. $

    Let $ \mu_h $ be the Haar measure. Then $ h_{\mu_h}(\tau) = h_{top}(\tau) $. Let $ \mu_h = \int_{\mathcal{M}^e(\mathbb{T}^m,\tau)}\nu d\rho(\nu) $ be the ergodic decomposition of $ \mu_h $. Then by Theorem 2.5, one has

    $ h_{top}(\tau) = \int_{\mathcal{M}^e(\mathbb{T}^m,\tau)}h_\nu(\tau) d\rho(\nu). $

    By variational principle, there exists $ \mu\in\mathcal{M}^e(\mathbb{T}^m,\tau) $ such that $ h_\mu(\tau) = h_{top}(\tau) $. Now we assume that $ a\in [0,h_{top}(\tau)) $. We have two cases.

    Case 1. $ A $ is quasi-hyperbolic. In this case, there is $ q\in\mathbb{T}^m $ such that $ A(q) = q-b $. We let

    $ \pi(x) = x-q\text{ for each }x\in\mathbb{T}^m. $

    Then $ \pi $ is a self homeomorphism of $ \mathbb{T}^m $ and $ \pi\circ\tau = A\circ\pi $. That is, $ (\mathbb{T}^m,\tau) $ topologically conjugates to a torus automorphism. By Quas and Soo's result [14,Theorem 1], there exists $ \mu_a\in\mathcal{M}^e(\mathbb{T}^m,\tau) $ such that $ h_{\mu_a}(\tau) = a $.

    Case 2. $ A $ is not quasi-hyperbolic. In this case, we put

    $ H = \{x\in\mathbb{T}^m:(A-id)^mx = 0\}. $

    Then $ H $ is a compact subgroup of $ \mathbb{T}^m $ and $ \mathbb{T}^m/H $ is a torus. We let $ Y = \mathbb{T}^m/H $ and $ \pi_Y $ be the natural projection from $ \mathbb{T}^m $ to $ Y $. The induced map $ \tau_Y $ on $ Y $ is a quasi-hyperbolic affine transformation and the extension $ \pi_Y $ is distal. Therefore, $ h_{top}(\tau_Y) = h_{top}(\tau) $ and by Case 1 there exists $ \mu^Y_a\in\mathcal{M}^e(Y,\tau_Y) $ such that $ h_{\mu^Y_a}(\tau_Y) = a $. There is $ \mu_a\in\mathcal{M}^e(\mathbb{T}^m,\tau) $ such that $ \pi_Y(\mu_a) = \mu^Y_a. $ Since the extension $ \pi_Y $ is distal, one has $ h_{\mu_a}(\tau) = h_{\mu^Y_a}(\tau_Y) = a $ (see [6,Theorem 4.4]).

    This ends the proof of Theorem 3.1.

    Let $ G $ be a group. For $ g, h\in G $, we write $ [g, h] = ghg^{-1}h^{-1} $ for the commutator of $ g $ and $ h $ and we write $ [B_1,B_2] $ for the subgroup spanned by $ \{[b_1,b_2] : b_1 \in B_1, b_2\in B_2\} $. The commutator subgroups $ G_j $, $ j\ge 1 $, are defined inductively by setting $ G_0 = G_1 = G $ and $ G_{j+1} = [G_j ,G] $. Let $ s \ge 1 $ be an integer. We say that $ G $ is $ s $-step nilpotent if $ G_{s+1} $ is the trivial subgroup. Recall that an $ s $-step nilmanifold is a manifold of the form $ G/\Gamma $ where $ G $ is a connected, simply connected $ s $-step nilpotent Lie group, and $ \Gamma $ is a cocompact discrete subgroup of $ G $.

    If $ G/\Gamma $ is an $ s $-step nilmanifold, then for each $ j = 1,\cdots,s $, $ G_j\Gamma $ and $ G_j $ are closed subgroups of $ G $ and $ G_j\Gamma/\Gamma $ is a closed submanifold of $ G/\Gamma $ (see Subsection 2.11 in [9]).

    We fix an $ s $-step nilmanifold of the form $ G/\Gamma $ and an affine transformation $ \tau $ of $ G/\Gamma $ such that

    $ \tau(g\Gamma) = g_0A(g)\Gamma\text{ for each } g\in G $

    where $ g_0\in G $ and $ A $ is a $ \Gamma $-invariant automorphism of $ G $. For each $ j\ge1 $, we let

    $ A_j: G_{j-1}\Gamma/G_{j}\Gamma\to G_{j-1}\Gamma/G_{j}\Gamma: A_j(hG_{j}\Gamma) = A(h)G_{j}\Gamma\text{ for each } h\in G_{j-1} $

    and

    $ \tau_j: G/G_{j}\Gamma\to G/G_{j}\Gamma: \tau_j(hG_{j}\Gamma) = g_0A(h)G_{j}\Gamma\text{ for each } h\in G. $

    It is easy to see that $ \{A_j\}_{j\in\mathbb{N}} $ and $ \{\tau_j\}_{j\in\mathbb{N}} $ are well defined since $ A(G_j)\subset G_j $ for each $ j\ge 1 $.

    For each $ j\ge 1 $, define the map $ \pi_{j+1} $ from $ G/G_{j+1}\Gamma $ to $ G/G_{j}\Gamma $ by

    $ πj+1(gGj+1Γ)=gGjΓ for each gG.
    $
    (3.1)

    It is easy to see that $ \pi_{j+1} $ is continuous and onto, and satisfies $ \pi_{j+1}\circ\tau_{j+1} = \tau_{j}\circ\pi_{j+1} $. Hence, for each $ j\ge 1 $, $ \pi_{j+1}:G/G_{j+1}\Gamma\to G/G_j\Gamma $ is a factor map. We let $ b_j = h_{top}(A_j) $ for each $ j\ge 1 $. Then we have the following.

    Lemma 3.2. For each $ j\ge 1 $ and $ y\in G/G_{j}\Gamma $, $ h_{d_{j+1}}(\tau_{j+1},\pi_{j+1}^{-1}(y)) = b_{j+1} $ where $ d_{j+1} $ is the metric on $ G/G_{j+1}\Gamma $.

    Proof. In Remark 2.4 (2), we let $ N = G_{j+1}\Gamma $ and $ H = G_{j}\Gamma $. Then both $ N $ and $ H $ are cocompact subgroup of $ G $. Moreover, $ N $ is a normal subgroup of $ H $. Hence $ (G/N = G/G_{j+1}\Gamma, \tau_{j+1}) $ is an $ (H/N = G_{j}\Gamma/G_{j+1}\Gamma, A_{j+1} ) $-extension of $ (G/H = G/G_{j}\Gamma, \tau_j) $. By (2.3), one has

    $ h_{d_{j+1}}(\tau_{j+1},\pi_{j+1}^{-1}(y)) = h_{top}(A_{j+1}) = b_{j+1}\text{ for every }y\in G/G_j\Gamma. $

    This ends the proof of Lemma 3.2.

    The following result is immediately from Lemma 3.2, (2.1) and Theorem 2.7.

    Lemma 3.3. For $ j\ge 1 $ and $ \nu_j\in \mathcal{M}(G/G_j\Gamma,\tau_j) $, there exists $ \mu\in\mathcal{M}(G/G_{j+1}\Gamma, \tau_{j+1}) $ such that $ h_{\mu}(\tau_{j+1}) = h_{\nu_j}(\tau_{j})+b_{j+1} $.

    We have the following.

    Corollary 3.4. $ h_{top}(\tau_j) = \sum_{i = 1}^jb_i $ for $ j\ge 1 $. Especially, $ h_{top}(\tau) = \sum_{i = 1}^{s+1}b_i $.

    Proof. We prove the corollary by induction on $ j $. In the case $ j = 1 $, it is obviously true. Now we assume that the corollary is valid for some $ j\in\mathbb{N} $. Then for $ j+1 $, let $ \pi_{j+1} $ be defined as in (3.1). Then by Ledrappier and Walters's result (2.1) and variational principle Theorem 2.2, we have

    $ htop(τj+1)=supμM(G/Gj+1Γ,τj+1)hμ(τj+1)supμM(G/GjΓ,τj)(hμ(τj)+G/GjΓhdj+1(τj+1,π1j+1(y))dμ(y))htop(τj)+supμM(G/GjΓ,τj)G/GjΓhdj+1(τj+1,π1j+1(y))dμ(y)=ji=1bi+bj+1=j+1i=1bi,
    $

    where we used Lemma 3.2. On the other hand, by Lemma 3.3 there exists $ \mu\in\mathcal{M}(G/G_{j+1}\Gamma,\tau_{j+1}) $ such that $ h_\mu(\tau_{j+1}) = \sum_{i = 1}^{j+1}b_i. $ Therefore $ h_{top}(\tau_{j+1}) = \sum_{i = 1}^{j+1}b_i. $ By induction, this ends the proof of Corollary 3.4.

    Remark 3.5. We remark that the topological entropy of $ (G/\Gamma,\tau) $ is determined by the associated matrix of $ \tau $ [1]. That is

    $ htop(τ)=hd(τ)=|λi|>1log|λi|
    $

    where $ \lambda_1,\lambda_2,\cdots,\lambda_m $ are the eigenvalues of the associated matrix of $ \tau $.

    Lemma 3.6. For $ j\ge 1 $ and $ \nu_j\in \mathcal{M}^e(G/G_j\Gamma,\tau_j) $, there is $ \nu_{j+1}\in\mathcal{M}^e(G/G_{j+1}\Gamma, \tau_{j+1}) $ such that $ h_{\nu_{j+1}}(\tau_{j+1}) = h_{\nu_j}(\tau_{j})+b_{j+1}. $

    Proof. We fix $ \nu_j\in\mathcal{M}^e(G/G_j\Gamma,\tau_j) $. Let $ \pi_{j+1} $ be defined as in (3.1). By Lemma 3.3, there exists $ \nu\in\mathcal{M}(G/G_{j+1}\Gamma,\tau_{j+1}) $ such that

    $ h_{\nu}(\tau_{j+1}) = \sup\limits_{\mu\in\mathcal{M}(G/G_{j+1}\Gamma,\tau_{j+1})\atop \pi_{j+1}(\mu) = \nu_{j}}h_{\mu}(\tau_{j+1}) = h_{\nu_j}(\tau_{j})+b_{j+1}. $

    We fix such $ \nu $ and assume that the ergodic decomposition of $ \nu $ is

    $ \nu = \int_{\mathcal{M}^e(G/G_{j+1}\Gamma,\tau_{j+1})}md\rho(m). $

    Then by property of ergodic decomposition, one has

    $ ρ({mMe(G/Gj+1Γ,τj+1):πj+1(m)=νj})=1.
    $

    Therefore, for $ \rho $-a.e. $ m\in\mathcal{M}^e(G/G_{j+1}\Gamma,\tau_{j+1}) $,

    $ h_m(\tau_{j+1})\le h_\nu(\tau_{j+1}) = h_{\nu_j}(\tau_{j})+b_{j+1}. $

    Hence by Theorem 2.5, one has

    $ h_{\nu_j}(\tau_{j})+b_{j+1} = h_\nu(\tau_{j+1}) = \int_{\mathcal{M}^e(G/G_{j+1}\Gamma,\tau_{j+1})}h_m(\tau_{j+1})d\rho(m)\le h_{\nu_j}(\tau_{j})+b_{j+1}. $

    We notice that the equality holds only in the case $ h_m(\tau_{j+1}) = h_{\nu_j}(\tau_{j})+b_{j+1} $ for $ \rho $-a.e. $ m\in\mathcal{M}^e(G/G_{j+1}\Gamma,\tau_{j+1}) $. Therefore, there exists $ \nu_{j+1}\in\mathcal{M}^e(G/G_{j+1}\Gamma,\tau_{j+1}) $ such that

    $ h_{\nu_{j+1}}(\tau_{j+1}) = h_{\nu_j}(\tau_{j})+b_{j+1}\text{ and }\pi_{j+1}(\nu_{j+1}) = \nu_j. $

    This ends the proof of Lemma 3.6.

    Now we are ready to prove our main results.

    Proof of Theorem 1.2. Firstly we assume that $ (G/\Gamma,\tau) $ has a fixed point $ p\Gamma $. We fix a real number $ a\in[0, h_{top}(\tau)] $. We are going to show that there exists $ \mu_a\in\mathcal{M}^e(G/\Gamma,\tau) $ such that $ h_{\mu_a}(\tau) = a $. By Corollary 3.4, we can find an $ i\in\{1,2,\cdots,s, s+1\} $ such that

    $ \sum\limits_{j = i+1}^{s+1}b_j\le a\le\sum\limits_{j = i}^{s+1}b_j. $

    Since $ p\Gamma $ is a fixed point of $ (G/\Gamma,\tau) $, there exists $ \gamma\in\Gamma $ such that $ g_0A(p) = p\gamma $. Therefore,

    $ \tau_{i}(pG_{i-1}\Gamma/G_{i}\Gamma) = p\gamma G_{i-1}\Gamma/G_{i}\Gamma\subset p[\gamma ,G_{i-1}]G_{i-1}\gamma\Gamma/G_{i}\Gamma\subset pG_{i-1}\Gamma/G_{i}\Gamma, $

    where we used the fact $ [\gamma,G_{i-1}]\subset G_{i-1} $. That is, $ (pG_{i-1}\Gamma/G_{i}\Gamma,\tau_i) $ is a TDS. We let

    $ \pi( phG_{i}\Gamma) = hG_{i}\Gamma\text{ for each } h\in G_{i-1}. $

    Then for each $ h\in G_{i-1} $, one has

    $ \pi\circ \tau_{i}(phG_{i}\Gamma) = p^{-1}g_0A(p)A(h)G_{i}\Gamma = \gamma A(h)G_{i}\Gamma = A(h)\gamma[\gamma,A(h)]G_{i}\Gamma = A(h)G_{i}\Gamma $

    where we used the fact $ [\gamma,A(h)]\in G_i $ since $ h\in G_{i-1} $. Therefore $ \pi\circ \tau_{i}(phG_{i}\Gamma) = A_i\circ\tau_i(phG_{i}\Gamma) $ for each $ h\in G_{i-1} $. That is $ \pi\circ \tau_{i} = A_{i}\circ\pi. $ Hence,

    $ (pG_{i-1}\Gamma/G_{i}\Gamma,\tau_{i})\text{ topologically conjugates to } (G_{i-1}\Gamma/G_{i}\Gamma, A_{i}). $

    Notice that $ (G_{i-1}\Gamma/G_{i}\Gamma, A_{i}) $ is a toral automarphism and $ h_{top}(A_{i}) = b_i $. By Theorem 3.1, there exists $ \nu_{i}\in\mathcal{M}^e(G/G_i\Gamma,\tau_{i}) $ such that $ h_{\nu_{i}}(\tau_{i}) = a-\sum_{j = i+1}^{s+1}b_j $. Combining this with Lemma 3.6, there exists an ergodic measure $ \mu_a = \nu_{s+1}\in\mathcal{M}^e(G/G_{s+1}\Gamma,\tau_{s+1}) = \mathcal{M}^e(G/\Gamma,\tau) $ such that

    $ h_{\mu_a}(\tau) = h_{\nu_{s+1}}(\tau_{s+1}) = h_{\nu_{i}}(\tau_{i})+\sum\limits_{j = i+1}^{s+1}b_j = a. $

    Thus $ \mu_a $ is the ergodic measure as required.

    Now we assume that $ (G/\Gamma,\tau) $ has a periodic point. By assumption, there exists $ m\in\mathbb{N} $ such that $ (G/\Gamma,\tau^m) $ has a fixed point. Since $ \tau^m $ is an affine transformation of $ G/\Gamma $, by argument above, there exists $ \mu\in\mathcal{M}^e(G/\Gamma,\tau^m) $ such that $ h_{\mu}(\tau^m) = ma $. Put $ \mu_a = \frac{1}{m}\sum_{j = 0}^{m-1}\tau^j(\mu) $. It is easy to see that $ \mu_a\in\mathcal{M}^e(G/\Gamma,\tau) $ and $ h_{\mu_a}(\tau) = \frac{h_\mu(\tau^m)}{m} = a $. Thus $ \mu_a $ is the ergodic measure as required.

    This ends the proof of Theorem 1.2.

    Proposition 3.7. Let $ G $ be an $ s $-step nilpotent Lie group and $ A $ be a quasi-hyperbolic automorphism of $ G $. Then for $ g\in G $, there exists $ p\in G $ such that $ gA(p) = p $.

    Proof. We prove the proposition by induction on $ s $. In the case $ s = 1 $, it is obviously true. Now we assume that the Proposition is valid in the case $ s = k $. Then in the case $ s = k+1 $, we fix $ g\in G $. Notice that $ G/G_{k+1} $ is a $ k $-step nilpotent Lie group. There exists $ \tilde p\in G $ such that $ gA(\tilde p)G_{k+1} = \tilde pG_{k+1} $. There exists $ \bar g\in G_{k+1} $ such that $ gA(\tilde p)\bar g = \tilde p $. There exists $ p'\in G_{k+1} $ such that $ \bar g^{-1}A(p') = p' $. In the end, we let $ p = \tilde p p' $. Then

    $ gA(p) = gA(\tilde p)A(p') = \tilde p \bar g^{-1}\bar g p' = \tilde pp' = p. $

    By induction, we end the proof of Proposition 3.7.

    Proof of Theorem 1.3. This comes immediately from Proposition 3.7 and Theorem 1.2.

    W. Huang was partially supported by NNSF of China (11731003, 12031019, 12090012). L. Xu was partially supported by NNSF of China (11801538, 11871188, 12031019) and the USTC Research Funds of the Double First-Class Initiative.

    [1] Forster DH, Daschner FD (1998) Acinetobacter species as nosocomial pathogens. Eur J Clin Microbiol Infect Dis 17: 73–77. doi: 10.1007/BF01682159
    [2] Cisneros JM, Rodriguez-Bano J (2002) Nosocomial bacteremia due to Acinetobacter baumannii: epidemiology, clinical features and treatment. Clin Microbiol Infect 8: 687–693. doi: 10.1046/j.1469-0691.2002.00487.x
    [3] Bonomo RA, Szabo D (2006) Mechanisms of multidrug resistance in Acinetobacter species and Pseudomonas aeruginosa. Clin Infect Dis 43 Suppl 2: S49–56.
    [4] Devaud M, Kayser FH, Bächi B (1982) Transposon-mediated multiple antibiotic resistance in Acinetobacter strains. Antimicrob Agents Chemother 22: 323–329. doi: 10.1128/AAC.22.2.323
    [5] Chu YW, Leung CM, Houang ET, et al. (1999) Skin carriage of Acinetobacters in Hong Kong. J Clin Microbiol 37: 2962–2967.
    [6] Jawad A, Snelling AM, Heritage J, et al. (1998) Exceptional desiccation tolerance of Acinetobacter radioresistens. J Hosp Infect 39: 235–240. doi: 10.1016/S0195-6701(98)90263-8
    [7] Dijkshoorn L, Nemec A, Seifert H (2007) An increasing threat in hospitals: multidrug-resistant Acinetobacter baumannii. Nat Rev Microbiol 5: 939–951. doi: 10.1038/nrmicro1789
    [8] Lopes JM, Goulart EM, Starling CE (2007) Pediatric mortality due to nosocomial infection: a critical approach. Braz J Infect Dis 11: 515–519.
    [9] Kurcik-Trajkovska B (2009) Acinetobacter spp. - A serious enemy threatening hospitals worldwide. Maced J Med Sci 2: 157–162.
    [10] La Scola B, Fournier PE, Brouqui P, et al. (2001) Detection and culture of Bartonella quintana, Serratia marcescens, and Acinetobacter spp. from decontaminated human body lice. J Clin Microbiol 39: 1707–1709.
    [11] Tomaras AP, Dorsey CW, Edelmann RE, et al. (2003) Attachment to and biofilm formation on abiotic surfaces by Acinetobacter baumannii: involvement of a novel chaperone-usher pili assembly system. Microbiology 149: 3473–3484. doi: 10.1099/mic.0.26541-0
    [12] Lee JC, Koerten H, van den Broek P, et al. (2006) Adherence of Acinetobacter baumannii strains to human bronchial epithelial cells. Res Microbiol 157: 360–366. doi: 10.1016/j.resmic.2005.09.011
    [13] Gospodarek E, Grzanka A, Dudziak Z, et al. (1998) Electron-microscopic observation of adherence of Acinetobacter baumannii to red blood cells. Acta Microbiol Pol 47: 213–217.
    [14] Costerton JW, Stewart PS, Greenberg EP (1999) Bacterial biofilms: a common cause of persistent infections. Science 284: 1318–1322. doi: 10.1126/science.284.5418.1318
    [15] Rao RS, Karthika RU, Singh SP, et al. (2008) Correlation between biofilm production and multiple drug resistance in imipenem resistant clinical isolates of Acinetobacter baumannii. Indian J Med Microbiol 26: 333–337. doi: 10.4103/0255-0857.43566
    [16] Carpentier B, Cerf O (1993) Biofilms and their consequences, with particular reference to hygiene in the food industry. J Appl Bacteriol 75: 499–511. doi: 10.1111/j.1365-2672.1993.tb01587.x
    [17] Gilbert P, Brown MR (1998) Biofilms and beta-lactam activity. J Antimicrob Chemother 41: 571–572. doi: 10.1093/jac/41.5.571
    [18] Hausner M, Wuertz S (1999) High rates of conjugation in bacterial biofilms as determined by quantitative in situ analysis. Appl Environ Microbiol 65: 3710–3713.
    [19] Otto M (2009) Staphylococcus epidermidis--the 'accidental' pathogen. Nat Rev Microbiol 7: 555–567. doi: 10.1038/nrmicro2182
    [20] Peleg AY, Seifert H, Paterson DL (2008) Acinetobacter baumannii: emergence of a successful pathogen. Clin Microbiol Rev 21: 538–582. doi: 10.1128/CMR.00058-07
    [21] Choi CH, Lee EY, Lee YC, et al. (2005) Outer membrane protein 38 of Acinetobacter baumannii localizes to the mitochondria and induces apoptosis of epithelial cells. Cell Microbiol 7: 1127–1138. doi: 10.1111/j.1462-5822.2005.00538.x
    [22] Loehfelm TW, Luke NR, Campagnari AA (2008) Identification and characterization of an Acinetobacter baumannii biofilm-associated protein. J Bacteriol 190: 1036–1044. doi: 10.1128/JB.01416-07
    [23] Choi AH, Slamti L, Avci FY, et al. (2009) The pgaABCD locus of Acinetobacter baumannii encodes the production of poly-beta-1-6-N-acetylglucosamine, which is critical for biofilm formation. J Bacteriol 191: 5953–5963. doi: 10.1128/JB.00647-09
    [24] Gaddy JA, Tomaras AP, Actis LA (2009) The Acinetobacter baumannii 19606 OmpA protein plays a role in biofilm formation on abiotic surfaces and in the interaction of this pathogen with eukaryotic cells. Infect Immun 77: 3150–3160. doi: 10.1128/IAI.00096-09
    [25] Kim SW, Choi CH, Moon DC, et al. (2009) Serum resistance of Acinetobacter baumannii through the binding of factor H to outer membrane proteins. FEMS Microbiol Lett 301: 224–231. doi: 10.1111/j.1574-6968.2009.01820.x
    [26] Cabral MP, Soares NC, Aranda J, et al. (2011) Proteomic and functional analyses reveal a unique lifestyle for Acinetobacter baumannii biofilms and a key role for histidine metabolism. J Proteome Res 10: 3399–3417. doi: 10.1021/pr101299j
    [27] Choi CH, Lee JS, Lee YC, et al. (2008) Acinetobacter baumannii invades epithelial cells and outer membrane protein A mediates interactions with epithelial cells. BMC Microbiol 8: 216. doi: 10.1186/1471-2180-8-216
    [28] Clemmer KM, Bonomo RA, Rather PN (2011) Genetic analysis of surface motility in Acinetobacter baumannii. Microbiology 157: 2534–2544. doi: 10.1099/mic.0.049791-0
    [29] Itoh Y, Rice JD, Goller C, et al. (2008) Roles of pgaABCD genes in synthesis, modification, and export of the Escherichia coli biofilm adhesin poly-beta-1,6-N-acetyl-D-glucosamine. J Bacteriol 190: 3670–3680. doi: 10.1128/JB.01920-07
    [30] Cramton SE, Gerke C, Schnell NF, et al. (1999) The intercellular adhesion (ica) locus is present in Staphylococcus aureus and is required for biofilm formation. Infect Immun 67: 5427–5433.
    [31] Kropec A, Maira-Litran T, Jefferson KK, et al. (2005) Poly-N-acetylglucosamine production in Staphylococcus aureus is essential for virulence in murine models of systemic infection. Infect Immun 73: 6868–6876. doi: 10.1128/IAI.73.10.6868-6876.2005
    [32] Lewis K (2001) Riddle of biofilm resistance. Antimicrob Agents Chemother 45: 999–1007. doi: 10.1128/AAC.45.4.999-1007.2001
    [33] Tomaras AP, Flagler MJ, Dorsey CW, et al. (2008) Characterization of a two-component regulatory system from Acinetobacter baumannii that controls biofilm formation and cellular morphology. Microbiology 154: 3398–3409. doi: 10.1099/mic.0.2008/019471-0
    [34] Luo LM, Wu LJ, Xiao YL, et al. (2015) Enhancing pili assembly and biofilm formation in Acinetobacter baumannii ATCC19606 using non-native acyl-homoserine lactones. BMC Microbiol 15: 62. doi: 10.1186/s12866-015-0397-5
    [35] Mussi MA, Limansky AS, Viale AM (2005) Acquisition of resistance to carbapenems in multidrug-resistant clinical strains of Acinetobacter baumannii: natural insertional inactivation of a gene encoding a member of a novel family of beta-barrel outer membrane proteins. Antimicrob Agents Chemother 49: 1432–1440. doi: 10.1128/AAC.49.4.1432-1440.2005
    [36] Poirel L, Lebessi E, Héritier C, et al. (2006) Nosocomial spread of OXA-58-positive carbapenem-resistant Acinetobacter baumannii isolates in a paediatric hospital in Greece. Clin Microbiol Infect 12: 1138–1141. doi: 10.1111/j.1469-0691.2006.01537.x
    [37] Aranda J, Bardina C, Beceiro A, et al. (2011) Acinetobacter baumannii RecA protein in repair of DNA damage, antimicrobial resistance, general stress response, and virulence. J Bacteriol 193: 3740–3747. doi: 10.1128/JB.00389-11
    [38] Diggle SP, Crusz SA, Camara M (2007) Quorum sensing. Curr Biol 17: R907–910. doi: 10.1016/j.cub.2007.08.045
    [39] Uroz S, Dessaux Y, Oger P (2009) Quorum sensing and quorum quenching: the yin and yang of bacterial communication. Chembiochem 10: 205–216. doi: 10.1002/cbic.200800521
    [40] Whitehead NA, Barnard AM, Slater H, et al. (2001) Quorum-sensing in Gram-negative bacteria. FEMS Microbiol Rev 25: 365–404. doi: 10.1111/j.1574-6976.2001.tb00583.x
    [41] Holden I, Swift I, Williams I (2000) New signal molecules on the quorum-sensing block. Trends Microbiol 8: 101–104; discussion 103–104. doi: 10.1016/S0966-842X(00)01718-2
    [42] Irie Y, Parsek MR (2008) Quorum sensing and microbial biofilms. Curr Top Microbiol Immunol 322: 67–84.
    [43] Williams P (2006) Quorum sensing. Int J Med Microbiol 296: 57–59. doi: 10.1016/j.ijmm.2006.01.034
    [44] Schaefer AL, Hanzelka BL, Eberhard A, et al. (1996) Quorum sensing in Vibrio fischeri: probing autoinducer-LuxR interactions with autoinducer analogs. J Bacteriol 178: 2897–2901.
    [45] González RH, Nusblat A, Nudel BC (2001) Detection and characterization of quorum sensing signal molecules in Acinetobacter strains. Microbiol Res 155: 271–277. doi: 10.1016/S0944-5013(01)80004-5
    [46] González RH, Dijkshoorn L, Van den Barselaar M, et al. (2009) Quorum sensing signal profile of Acinetobacter strains from nosocomial and environmental sources. Rev Argent Microbiol 41: 73–78.
    [47] Prashanth K, Vasanth T, Saranathan R, et al. (2012) Antibiotic resistance, biofilms and quorum 487 sensing in Acinetobacter species, In: Antibiotic resistant bacteria - A coninuous challenge in the 488 new millennium, Dr. Marina Pana (Ed.); Croatia : InTech, 179–212.
    [48] Niu C, Clemmer KM, Bonomo RA, et al. (2008) Isolation and characterization of an autoinducer synthase from Acinetobacter baumannii. J Bacteriol 190: 3386–3392. doi: 10.1128/JB.01929-07
    [49] Stevens AM, Dolan KM, Greenberg EP (1994) Synergistic binding of the Vibrio fischeri LuxR transcriptional activator domain and RNA polymerase to the lux promoter region. Proc Natl Acad Sci U S A 91: 12619–12623. doi: 10.1073/pnas.91.26.12619
    [50] Egland KA, Greenberg EP (2001) Quorum sensing in Vibrio fischeri: analysis of the LuxR DNA binding region by alanine-scanning mutagenesis. J Bacteriol 183: 382–386. doi: 10.1128/JB.183.1.382-386.2001
    [51] Latifi A, Winson MK, Foglino M, et al. (1995) Multiple homologues of LuxR and LuxI control expression of virulence determinants and secondary metabolites through quorum sensing in Pseudomonas aeruginosa PAO1. Mol Microbiol 17: 333–343. doi: 10.1111/j.1365-2958.1995.mmi_17020333.x
    [52] Gray KM, Garey JR (2001) The evolution of bacterial LuxI and LuxR quorum sensing regulators. Microbiology 147: 2379–2387. doi: 10.1099/00221287-147-8-2379
    [53] Bhargava N, Sharma P, Capalash N (2010) Quorum sensing in Acinetobacter: an emerging pathogen. Crit Rev Microbiol 36: 349-360. doi: 10.3109/1040841X.2010.512269
    [54] Surette MG, Miller MB, Bassler BL (1999) Quorum sensing in Escherichia coli, Salmonella typhimurium, and Vibrio harveyi: a new family of genes responsible for autoinducer production. Proc Natl Acad Sci U S A 96: 1639–1644. doi: 10.1073/pnas.96.4.1639
    [55] Young DM, Parke D, Ornston LN (2005) Opportunities for genetic investigation afforded by Acinetobacter baylyi, a nutritionally versatile bacterial species that is highly competent for natural transformation. Annu Rev Microbiol 59: 519–551. doi: 10.1146/annurev.micro.59.051905.105823
    [56] Smith MG, Gianoulis TA, Pukatzki S, et al. (2007) New insights into Acinetobacter baumannii pathogenesis revealed by high-density pyrosequencing and transposon mutagenesis. Genes Dev 21: 601–614. doi: 10.1101/gad.1510307
    [57] Oh MH, Choi CH (2015) Role of LuxIR homologue AnoIR in Acinetobacter nosocomialis and the effect of virstatin on the expression of anoR Gene. J Microbiol Biotechnol 25: 1390–1400. doi: 10.4014/jmb.1504.04069
    [58] Taccone FS, Rodriguez-Villalobos H, De Backer D, et al. (2006) Successful treatment of septic shock due to pan-resistant Acinetobacter baumannii using combined antimicrobial therapy including tigecycline. Eur J Clin Microbiol Infect Dis 25: 257–260. doi: 10.1007/s10096-006-0123-1
    [59] Valencia R, Arroyo LA, Conde M, et al. (2009) Nosocomial outbreak of infection with pan-drug-resistant Acinetobacter baumannii in a tertiary care university hospital. Infect Control Hosp Epidemiol 30: 257–263. doi: 10.1086/595977
    [60] Amaral L, Martins A, Spengler G, et al. (2014) Efflux pumps of Gram-negative bacteria: what they do, how they do it, with what and how to deal with them. Front Pharmacol 4: 168.
    [61] Balaban N, Cirioni O, Giacometti A, et al. (2007) Treatment of Staphylococcus aureus biofilm infection by the quorum-sensing inhibitor RIP. Antimicrob Agents Chemother 51: 2226–2229. doi: 10.1128/AAC.01097-06
    [62] Hoffman LR, D'Argenio DA, MacCoss MJ, et al. (2005) Aminoglycoside antibiotics induce bacterial biofilm formation. Nature 436: 1171–1175. doi: 10.1038/nature03912
    [63] Henikoff S, Wallace JC, Brown JP (1990) Finding protein similarities with nucleotide sequence databases. Methods Enzymol 183: 111–132. doi: 10.1016/0076-6879(90)83009-X
    [64] Rahmati S, Yang S, Davidson AL, et al. (2002) Control of the AcrAB multidrug efflux pump by quorum-sensing regulator SdiA. Mol Microbiol 43: 677–685. doi: 10.1046/j.1365-2958.2002.02773.x
    [65] Maseda H, Sawada I, Saito K, et al. (2004) Enhancement of the mexAB-oprM efflux pump expression by a quorum-sensing autoinducer and its cancellation by a regulator, MexT, of the mexEF-oprN efflux pump operon in Pseudomonas aeruginosa. Antimicrob Agents Chemother 48: 1320–1328. doi: 10.1128/AAC.48.4.1320-1328.2004
    [66] Chu YW, Chau SL, Houang ET (2006) Presence of active efflux systems AdeABC, AdeDE and AdeXYZ in different Acinetobacter genomic DNA groups. J Med Microbiol 55: 477–478. doi: 10.1099/jmm.0.46433-0
    [67] Nemec A, Maixnerova M, van der Reijden TJ, et al. (2007) Relationship between the AdeABC efflux system gene content, netilmicin susceptibility and multidrug resistance in a genotypically diverse collection of Acinetobacter baumannii strains. J Antimicrob Chemother 60: 483–489. doi: 10.1093/jac/dkm231
    [68] Yoon EJ, Courvalin P, Grillot-Courvalin C (2013) RND-type efflux pumps in multidrug-resistant clinical isolates of Acinetobacter baumannii: major role for AdeABC overexpression and AdeRS mutations. Antimicrob Agents Chemother 57: 2989–2995. doi: 10.1128/AAC.02556-12
    [69] Coyne S, Courvalin P, Périchon B (2011) Efflux-mediated antibiotic resistance in Acinetobacter spp. Antimicrob Agents Chemother 55: 947–953. doi: 10.1128/AAC.01388-10
    [70] He X, Lu F, Yuan F, et al. (2015) Biofilm formation caused by clinical Acinetobacter baumannii isolates is associated with overexpression of the AdeFGH Efflux pump. Antimicrob Agents Chemother 59: 4817–4825. doi: 10.1128/AAC.00877-15
    [71] Kayama S, Murakami K, Ono T, et al. (2009) The role of rpoS gene and quorum-sensing system in ofloxacin tolerance in Pseudomonas aeruginosa. FEMS Microbiol Lett 298: 184–192. doi: 10.1111/j.1574-6968.2009.01717.x
    [72] Que YA, Hazan R, Strobel B, et al. (2013) A quorum sensing small volatile molecule promotes antibiotic tolerance in bacteria. PLoS One 8: e80140. doi: 10.1371/journal.pone.0080140
    [73] Khan MS, Zahin M, Hasan S, et al. (2009) Inhibition of quorum sensing regulated bacterial functions by plant essential oils with special reference to clove oil. Lett Appl Microbiol 49: 354–360. doi: 10.1111/j.1472-765X.2009.02666.x
    [74] Sperandio V (2007) Novel approaches to bacterial infection therapy by interfering with bacteria-to-bacteria signaling. Expert Rev Anti Infect Ther 5: 271–276. doi: 10.1586/14787210.5.2.271
    [75] Stacy DM, Welsh MA, Rather PN, et al. (2012) Attenuation of quorum sensing in the pathogen Acinetobacter baumannii using non-native N-Acyl homoserine lactones. ACS Chem Biol 7: 1719–1728. doi: 10.1021/cb300351x
    [76] Saroj SD, Rather PN (2013) Streptomycin inhibits quorum sensing in Acinetobacter baumannii. Antimicrob Agents Chemother 57: 1926–1929. doi: 10.1128/AAC.02161-12
    [77] Chabane YN, Mlouka MB, Alexandre S, et al. (2014) Virstatin inhibits biofilm formation and motility of Acinetobacter baumannii. BMC Microbiol 14: 62. doi: 10.1186/1471-2180-14-62
    [78] Choo JH, Rukayadi Y, Hwang JK (2006) Inhibition of bacterial quorum sensing by vanilla extract. Lett Appl Microbiol 42: 637–641.
    [79] Rasmussen TB, Bjarnsholt T, Skindersoe ME, et al. (2005) Screening for quorum-sensing inhibitors (QSI) by use of a novel genetic system, the QSI selector. J Bacteriol 187: 1799–1814. doi: 10.1128/JB.187.5.1799-1814.2005
    [80] Cady NC, McKean KA, Behnke J, et al. (2012) Inhibition of biofilm formation, quorum sensing and infection in Pseudomonas aeruginosa by natural products-inspired organosulfur compounds. PLoS One 7: e38492. doi: 10.1371/journal.pone.0038492
    [81] Sambanthamoorthy K, Luo C, Pattabiraman N, et al. (2014) Identification of small molecules inhibiting diguanylate cyclases to control bacterial biofilm development. Biofouling 30: 17–28. doi: 10.1080/08927014.2013.832224
    [82] Dong YH, Wang LH, Xu JL, et al. (2001) Quenching quorum-sensing-dependent bacterial infection by an N-acyl homoserine lactonase. Nature 411: 813–817. doi: 10.1038/35081101
    [83] Chow JY, Yang Y, Tay SB, et al. (2014) Disruption of biofilm formation by the human pathogen Acinetobacter baumannii using engineered quorum-quenching lactonases. Antimicrob Agents Chemother 58: 1802–1805. doi: 10.1128/AAC.02410-13
    [84] Hoang TT, Schweizer HP (1999) Characterization of Pseudomonas aeruginosa enoyl-acyl carrier protein reductase (FabI): a target for the antimicrobial triclosan and its role in acylated homoserine lactone synthesis. J Bacteriol 181: 5489–5497.
    [85] Jarrett CO, Deak E, Isherwood KE, et al. (2004) Transmission of Yersinia pestis from an infectious biofilm in the flea vector. J Infect Dis 190: 783–792. doi: 10.1086/422695
    [86] Czajkowski R, Jafra S (2009) Quenching of acyl-homoserine lactone-dependent quorum sensing by enzymatic disruption of signal molecules. Acta Biochim Pol 56: 1–16.
    [87] Lin YH, Xu JL, Hu J, et al. (2003) Acyl-homoserine lactone acylase from Ralstonia strain XJ12B represents a novel and potent class of quorum-quenching enzymes. Mol Microbiol 47: 849–860. doi: 10.1046/j.1365-2958.2003.03351.x
    [88] Romero M, Diggle SP, Heeb S, et al. (2008) Quorum quenching activity in Anabaena sp. PCC 7120: identification of AiiC, a novel AHL-acylase. FEMS Microbiol Lett 280: 73–80.
    [89] Uroz S, Oger PM, Chapelle E, et al. (2008) A Rhodococcus qsdA-encoded enzyme defines a novel class of large-spectrum quorum-quenching lactonases. Appl Environ Microbiol 74: 1357–1366. doi: 10.1128/AEM.02014-07
    [90] Chow JY, Xue B, Lee KH, et al. (2010) Directed evolution of a thermostable quorum-quenching lactonase from the amidohydrolase superfamily. J Biol Chem 285: 40911–40920. doi: 10.1074/jbc.M110.177139
    [91] Kiran S (2011) Enzymatic quorum quenching increases antibiotic susceptibility of multidrug resistant Pseudomonas aeruginosa. Irani J Microbiol 3: 1–12.
    [92] Limsuwan S, Subhadhirasakul S, Voravuthikunchai PS (2009) Medicinal plants with significant activity against important pathogenic bacteria. Pharm Biol 47: 683–689. doi: 10.1080/13880200902930415
    [93] Babić F, Venturi V, Maravić-Vlahoviček G (2010) Tobramycin at subinhibitory concentration inhibits the RhlI/R quorum sensing system in a Pseudomonas aeruginosa environmental isolate. BMC Infect Dis 10: 148. doi: 10.1186/1471-2334-10-148
    [94] Defoirdt T, Boon N, Bossier P (2010) Can bacteria evolve resistance to quorum sensing disruption? PLoS Pathog 6: e1000989. doi: 10.1371/journal.ppat.1000989
  • This article has been cited by:

    1. XIAOBO HOU, XUETING TIAN, Conditional intermediate entropy and Birkhoff average properties of hyperbolic flows, 2024, 44, 0143-3857, 2257, 10.1017/etds.2023.110
    2. Peng Sun, Ergodic measures of intermediate entropies for dynamical systems with the approximate product property, 2025, 465, 00018708, 110159, 10.1016/j.aim.2025.110159
    3. Yi Shi, Xiaodong Wang, Measures of intermediate pressures for geometric Lorenz attractors, 2025, 436, 00220396, 113280, 10.1016/j.jde.2025.113280
  • Reader Comments
  • © 2016 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0)
通讯作者: 陈斌, bchen63@163.com
  • 1. 

    沈阳化工大学材料科学与工程学院 沈阳 110142

  1. 本站搜索
  2. 百度学术搜索
  3. 万方数据库搜索
  4. CNKI搜索

Metrics

Article views(11171) PDF downloads(1855) Cited by(29)

Figures and Tables

Figures(1)

Other Articles By Authors

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return

Catalog