Neutrophil Dynamics in Mycobacterial Infections
Summary
Neutrophils represent a frontline defence in mycobacterial infections, contributing both to pathogen containment and to host pathology. Upon inhalation of Mycobacterium tuberculosis and related species, neutrophils are rapidly recruited to the pulmonary environment, where they engage in phagocytosis, degranulation and production of reactive oxygen species. This effector repertoire can limit bacterial dissemination yet also promote tissue damage. Within developing granulomas, neutrophils assume diverse phenotypes, ranging from immature, permissive subsets that may foster pathogen survival to hyperactivated cells that release inflammatory mediators. The formation of neutrophil extracellular traps (NETs) further exemplifies this duality: NETs can ensnare bacilli but excessive trap formation is associated with caseation and vascular occlusion. Recent efforts in immunometabolism have revealed that neutrophil functional states are regulated by metabolic pathways such as glycolysis and fatty acid oxidation, offering potential avenues for host-directed therapies. Interactions with other myeloid cells, especially monocytes and macrophages, shape neutrophil accumulation and phenotypic differentiation, with intricate feedback loops dictating protective immunity or immunopathology. Understanding these dynamics is essential for the development of diagnostic markers and for interventions aimed at balancing microbial control with preservation of lung integrity.
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Neutrophil Dynamics in Mycobacterial Infections publication trend
The graph below shows the total number of articles in neutrophil dynamics in mycobacterial infections across all publications each year (not limited to Nature Index journals).
Technical terms
Neutrophil extracellular traps (NETs): Web-like DNA structures decorated with antimicrobial proteins, released by activated neutrophils to trap pathogens.
Granuloma: Organized immune structure comprising macrophages, lymphocytes and neutrophils that contains persistent pathogens.
ESX-1 type VII secretion system: A specialised protein export apparatus in pathogenic mycobacteria essential for virulence and host cell modulation.
Fatty acid oxidation (FAO): Metabolic pathway in mitochondria that breaks down fatty acids to generate energy and regulate immune cell functions.
Immunopathology: Tissue damage arising from host immune responses rather than direct microbial action.
References
- Neutrophil extracellular traps characterize caseating granulomas. Cell Death & Disease (2024).
- Fatty acid metabolism in neutrophils promotes lung damage and bacterial replication during tuberculosis. PLOS Pathogens (2024).
- Intragranuloma Accumulation and Inflammatory Differentiation of Neutrophils Underlie Mycobacterial ESX-1-Dependent Immunopathology. mBio (2023).
- Mycobacterium tuberculosis in a Trap: The Role of Neutrophil Extracellular Traps in Tuberculosis. International Journal of Molecular Sciences (2023).
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