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Neutrophils in Tuberculosis-Associated Inflammation and Lung Pathology

Protective immunity to Mycobacterium tuberculosis (Mtb)—the causative agent of tuberculosis (TB)—is not fully understood but involves immune responses within the pulmonary airways which can lead to exacerbated inflammation and immune pathology. In humans, this inflammation results in lung damage; th...

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Detalles Bibliográficos
Autores principales: Muefong, Caleb N., Sutherland, Jayne S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7266980/
https://www.ncbi.nlm.nih.gov/pubmed/32536917
http://dx.doi.org/10.3389/fimmu.2020.00962
Descripción
Sumario:Protective immunity to Mycobacterium tuberculosis (Mtb)—the causative agent of tuberculosis (TB)—is not fully understood but involves immune responses within the pulmonary airways which can lead to exacerbated inflammation and immune pathology. In humans, this inflammation results in lung damage; the extent of which depends on specific host pro-inflammatory processes. Neutrophils, though increasingly linked to the development of inflammatory disorders, have been less well studied in relation to TB-induced lung pathology. Neutrophils mode of action and their specialized functions can be directly linked to TB-specific lung tissue damage observed on patient chest X-rays at diagnosis and contribute to long-term pulmonary sequelae. This review discusses aspects of neutrophil activity associated with active TB, including the resulting inflammation and pulmonary impairment. It highlights the significance of neutrophil function on TB disease outcome and underlines the necessity of monitoring neutrophil function for better assessment of the immune response and severity of lung pathology associated with TB. Finally, we propose that some MMPs, ROS, MPO, S100A8/A9 and Glutathione are neutrophil-related inflammatory mediators with promising potential as targets for developing host-directed therapies for TB.