Mycobacterial Infection and Host Immune Responses
Summary
Infection by Mycobacterium species, most notably Mycobacterium tuberculosis, remains a leading cause of morbidity and mortality worldwide. Transmission occurs via inhalation of aerosolised bacilli, which initially encounter alveolar macrophages and epithelial cells in the lung. Recognition of pathogen-associated molecular patterns by toll-like receptors and other pattern recognition receptors triggers secretion of cytokines such as tumour necrosis factor, interleukin-1 and interferon-γ. These mediators coordinate the recruitment of neutrophils and monocytes, and prime macrophages for enhanced microbicidal activity. Successful containment of infection often results in granuloma formation, a structured aggregate of activated immune cells that walls off bacilli but may also harbour latent organisms. Adaptive immunity, particularly Th1 CD4+ T cells and cytotoxic CD8+ T cells, is essential for long-term control. Mycobacteria deploy multiple evasion strategies, including inhibition of phagosome maturation, modulation of host lipid metabolism and entry into metabolic dormancy. The global rise of drug-resistant strains and the complex interplay between host and pathogen have driven innovation in experimental models and host-directed therapies aimed at restoring effective immune clearance without exacerbating tissue damage.
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Mycobacterial Infection and Host Immune Responses publication trend
The graph below shows the total number of articles in mycobacterial infection and host immune responses across all publications each year (not limited to Nature Index journals).
Technical terms
Alveolar macrophage: Resident lung phagocyte that engulfs inhaled mycobacteria and initiates immune responses.
Alveolar epithelial cell: Type I and II lung lining cells that provide a barrier and contribute to immune signalling.
Granuloma: Structured aggregate of immune cells that contains mycobacterial infection but may harbour latent bacilli.
Cytokine: Small secreted protein that regulates cell communication and directs immune responses.
Chemokine: Subset of cytokines that direct migration of immune cells to sites of infection.
Organoid: Three-dimensional tissue culture model that mimics organ structure and function.
Host-directed therapy: Treatment strategy aiming to enhance immune mechanisms rather than target the pathogen directly.
References
- Advances in an In Vitro Tuberculosis Infection Model Using Human Lung Organoids for Host-Directed Therapies. PLOS Pathogens (2024).
- Airway epithelial cells mount an early response to mycobacterial infection. Frontiers in Cellular and Infection Microbiology (2023).
- Impact of the elderly lung mucosa on Mycobacterium tuberculosis transcriptional adaptation during infection of alveolar epithelial cells. Microbiology Spectrum (2024).
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