Research article Topical Sections

Tumor necrosis factor (TNF) induces astrogliosis, microgliosis and promotes survival of cortical neurons

  • Received: 18 July 2021 Accepted: 02 November 2021 Published: 16 November 2021
  • Objectives

    Neuro-inflammation occurs as a sequence of brain injury and is associated with production of cytokines. Cytokines can modulate the function and survival of neurons, microglia and astrocytes. The objective of this study is to examine the effect of TNF on the neurons, microglia and astrocytes in normal brain and stab wound brain injury.

    Methods

    Normal BALB/c male mice (N) without any injury were subdivided into NA and NB groups. Another set mouse was subjected to stab wound brain injury (I) and were subdivided into IA and IB. NA and IA groups received intraperitoneal injections of TNF (1 µg/kg body weight/day) for nine days, whereas NB and IB groups received intraperitoneal injections of PBS. Animals were killed on 1st, 2nd, 3rd, 7th, and 9th day. Frozen brain sections through the injury site in IA and IB or corresponding region in NA and NB groups were stained for neurodegeneration, immunostained for astrocytes, microglia and neurons. Western blotting for GFAP and ELISA for BDNF were done from the tissues collected from all groups.

    Results

    The number of degenerating neurons significantly decreased in TNF treated groups. There was a significant increase in the number of astrocytes and microglia in TNF treated groups compared to PBS treated groups. In addition, it was found that TNF stimulated the expression of GFAP and BDNF in NA and IA groups.

    Conclusions

    TNF induces astrogliosis and microgliosis in normal and injured brain and promotes the survival of cortical neurons in stab wound brain injury, may be by upregulating the BDNF level.

    Citation: Ebtesam M Abd-El-Basset, Muddanna Sakkattu Rao, Solaiman M Alshawaf, Hasan Kh Ashkanani, Abdulaziz H Kabli. Tumor necrosis factor (TNF) induces astrogliosis, microgliosis and promotes survival of cortical neurons[J]. AIMS Neuroscience, 2021, 8(4): 558-584. doi: 10.3934/Neuroscience.2021031

    Related Papers:

  • Objectives

    Neuro-inflammation occurs as a sequence of brain injury and is associated with production of cytokines. Cytokines can modulate the function and survival of neurons, microglia and astrocytes. The objective of this study is to examine the effect of TNF on the neurons, microglia and astrocytes in normal brain and stab wound brain injury.

    Methods

    Normal BALB/c male mice (N) without any injury were subdivided into NA and NB groups. Another set mouse was subjected to stab wound brain injury (I) and were subdivided into IA and IB. NA and IA groups received intraperitoneal injections of TNF (1 µg/kg body weight/day) for nine days, whereas NB and IB groups received intraperitoneal injections of PBS. Animals were killed on 1st, 2nd, 3rd, 7th, and 9th day. Frozen brain sections through the injury site in IA and IB or corresponding region in NA and NB groups were stained for neurodegeneration, immunostained for astrocytes, microglia and neurons. Western blotting for GFAP and ELISA for BDNF were done from the tissues collected from all groups.

    Results

    The number of degenerating neurons significantly decreased in TNF treated groups. There was a significant increase in the number of astrocytes and microglia in TNF treated groups compared to PBS treated groups. In addition, it was found that TNF stimulated the expression of GFAP and BDNF in NA and IA groups.

    Conclusions

    TNF induces astrogliosis and microgliosis in normal and injured brain and promotes the survival of cortical neurons in stab wound brain injury, may be by upregulating the BDNF level.



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    Acknowledgments



    This work was supported by the Kuwait University and OMICS RU under Grant (Number-CSRUL02/13). Authors would like to acknowledge Animal Resources Centre (ARC) for providing mice and animal house facility. We also thank Mrs Amna Najem for her technical assistance.

    Conflict of interest



    All authors declare no conflicts of interest.

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