Crosstalk between Microglia and Neurons in Neurotrauma: An Overview of the Underlying Mechanisms

Authors

Muhammad Ali Haidar, Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Stanley Ibeh, Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Zaynab Shakkour, Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Mohammad Amine Reslan, Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Judith Nwaiwu, Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Yomna Adel Moqidem, Biotechnology Program, School of Science and Engineering, The American University in Cairo, Cairo, Egypt.
Georgio Sader, Faculty of Medicine, University of Balamand, Balamand, Lebanon.
Rachel G. Nickles, Program for Neurotrauma, Neuroproteomics & Biomarkers Research, Departments of Emergency Medicine, University of Florida, Gainesville, FL 32611, USA.
Ismail Babale, Department of Biomedical Engineering, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Aneese A. Jaffa, Department of Biology, Faculty of Arts and Sciences, American University of Beirut, Beirut, Lebanon.
Mohamed Salama, Institute of Global Health and Human Ecology (I-GHHE), The American University in Cairo, New Cairo 11835, Egypt.
Abdullah Shaito, Biomedical Research Center, Qatar University, P.O. Box 2713, Doha, Qatar.
Firas Kobeissy, Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.

Fifth Author's Department

Biotechnology Program

Document Type

Research Article

Publication Title

Current neuropharmacology

Publication Date

1-1-2022

doi

10.2174/1570159X19666211202123322

Abstract

Microglia are the resident immune cells of the brain and play a crucial role in housekeeping and maintaining homeostasis of the brain microenvironment. Upon injury or disease, microglial cells become activated, at least partly, via signals initiated by injured neurons. Activated microglia, thereby, contribute to both neuroprotection and neuroinflammation. However, sustained microglial activation initiates a chronic neuroinflammatory response which can disturb neuronal health and disrupt communications between neurons and microglia. Thus, microglia-neuron crosstalk is critical in a healthy brain as well as during states of injury or disease. As most studies focus on how neurons and microglia act in isolation during neurotrauma, there is a need to understand the interplay between these cells in brain pathophysiology. This review highlights how neurons and microglia reciprocally communicate under physiological conditions and during brain injury and disease. Furthermore, the modes of microglia-neuron communication are exposed, focusing on cell-contact dependent signaling and communication by the secretion of soluble factors like cytokines and growth factors. In addition, it has been discussed that how microglia-neuron interactions could exert either beneficial neurotrophic effects or pathologic proinflammatory responses. We further explore how aberrations in microglia-neuron crosstalk may be involved in central nervous system (CNS) anomalies, namely traumatic brain injury (TBI), neurodegeneration, and ischemic stroke. A clear understanding of how the microglia-neuron crosstalk contributes to the pathogenesis of brain pathologies may offer novel therapeutic avenues of brain trauma treatment.

First Page

2050

Last Page

2065

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