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Potential of Neuroinflammation-Modulating Strategies in Tuberculous Meningitis: Targeting Microglia
Huan-Jun Lu1, Daji Guo2, Qian-Qi Wei3
1Institute of Special Environmental Medicine, Nantong University, Jiangsu, China.
Abstract:
Tuberculous meningitis (TBM) is the most severe complication of tuberculosis (TB) and is associated with high rates of disability and mortality. Mycobacterium tuberculosis (M. tb), the infectious agent of TB, disseminates from the respiratory epithelium, breaks through the blood-brain barrier, and establishes a primary infection in the meninges. Microglia are the core of the immune network in the central nervous system (CNS) and interact with glial cells and neurons to fight against harmful pathogens and maintain homeostasis in the brain through pleiotropic functions. However, M. tb directly infects microglia and resides in them as the primary host for bacillus infections. Largely, microglial activation slows disease progression. The non-productive inflammatory response that initiates the secretion of pro-inflammatory cytokines and chemokines may be neurotoxic and aggravate tissue injuries based on damages caused by M. tb. Host-directed therapy (HDT) is an emerging strategy for modulating host immune responses against diverse diseases. Recent studies have shown that HDT can control neuroinflammation in TBM and act as an adjunct therapy to antibiotic treatment. In this review, we discuss the diverse roles of microglia in TBM and potential host-directed TB therapies that target microglia to treat TBM. We also discuss the limitations of applying each HDT and suggest a course of action for the near future.
Insights
Tuberculous meningitis (TBM) involves Mycobacterium tuberculosis infecting microglia in the brain. Host-directed therapies targeting these immune cells show promise for treating TBM alongside antibiotics.
Area of Science:
- Neuroscience
- Immunology
- Infectious Diseases
Background:
- Tuberculous meningitis (TBM) is a severe complication of tuberculosis (TB) with significant mortality and disability.
- Mycobacterium tuberculosis (M. tb) invades the central nervous system (CNS) by crossing the blood-brain barrier.
- Microglia, the primary immune cells of the CNS, are crucial in TBM pathogenesis and serve as the main host for M. tb within the brain.
Purpose of the Study:
- To review the multifaceted roles of microglia in TBM.
- To explore potential host-directed therapies (HDTs) targeting microglia for TBM treatment.
- To discuss limitations and future directions for HDTs in TBM.
Main Methods:
- Literature review of studies on microglia in TBM.
- Analysis of current and emerging host-directed therapeutic strategies.
- Discussion of the neuroinflammatory and neurotoxic mechanisms in TBM.
Main Results:
- Microglial activation can initially slow TBM progression but may lead to detrimental neuroinflammation.
- M. tb directly infects microglia, establishing a persistent infection.
- HDTs demonstrate potential in controlling neuroinflammation and can complement antibiotic treatments for TBM.
Conclusions:
- Microglia play a dual role in TBM, influencing both disease progression and host response.
- Targeting microglia with HDTs represents a promising adjunctive strategy for TBM management.
- Further research is needed to overcome limitations and optimize HDT application in TBM.
