Abstract
The mycobacterium genus contains a broad range of species, including the human pathogens M. tuberculosis and M. leprae. These bacteria are best known for their residence inside host cells. Neutrophils are frequently observed at sites of mycobacterial infection, but their role in clearance is not well understood. In this review, we discuss how neutrophils attempt to control mycobacterial infections, either through the ingestion of bacteria into intracellular phagosomes, or the release of neutrophil extracellular traps (NETs). Despite their powerful antimicrobial activity, including the production of reactive oxidants such as hypochlorous acid, neutrophils appear ineffective in killing pathogenic mycobacteria. We explore mycobacterial resistance mechanisms, and how thwarting neutrophil action exacerbates disease pathology. A better understanding of how mycobacteria protect themselves from neutrophils will aid the development of novel strategies that facilitate bacterial clearance and limit host tissue damage.
Highlights
Mycobacterium is a diverse genus comprising almost 200 species [1]
We have shown that M. smegmatis can cope with relatively high doses of the most bactericidal oxidant produced in the neutrophil phagosome, hypochlorous acid (HOCl) (LD50 of 90 nmol/108 CFU) [127]
While neutrophils attempt to control mycobacterial infection, the bulk of the evidence indicates that the effectiveness of their phagosomal and extracellular killing mechanisms is thwarted by the microbes
Summary
Parker , Lorna Forrester , Christopher D. Kaldor , Nina Dickerhof and Mark B. Specialty section: This article was submitted to Molecular Innate Immunity, a section of the journal
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