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Published on: September 27, 2018
Export of eDNA is a mechanism used by Mycobacterium avium subsp. hominissuis for survival within host macrophages
Jayanthi J Joseph1,2, Amy Leestemaker-Palmer1, Luiz E Bermudez3,4
1Department of Biomedical Sciences, Carlson College of Veterinary Medicine, Corvallis, USA.
Abstract:
Mycobacterium avium subsp. hominissuis (M. avium) is a pathogen that causes pulmonary and systemic infection in humans. Mycobacterial infection activates both pro-inflammatory and anti-inflammatory pathways modulating these routes to escape killing. eDNA has a role for environmental survival and biofilm formation of M. avium. We hypothesized that M. avium eDNA might play a role in macrophages survival. To investigate the macrophage response to M. avium eDNA, we utilized two virulent strains of M. avium, eDNA-deficient mutants, and nonvirulent Mycobacterium smegmatis. eDNA-deficient mutants were attenuated at macrophage survival and yielded significantly higher IL-1β than wildtype bacterium, while M. avium, but not M. smegmatis, suppresses IL-1β production and NLRP3 expression by host macrophages. We also observed that M. avium triggered IFN-β production in a DNA-dependent manner but did not have an effect on cGAS expression. These data indicate that M. avium strains modulate macrophage responses in an eDNA dependent manner.
Insights
Extracellular DNA (eDNA) from Mycobacterium avium subsp. hominissuis helps the pathogen survive within macrophages. Removing eDNA boosts IL-1β production, indicating a key role for eDNA in immune evasion.
Area of Science:
- Immunology
- Microbiology
- Molecular Biology
Background:
- Mycobacterium avium subsp. hominissuis (M. avium) causes human infections.
- M. avium manipulates host inflammatory pathways for survival.
- Extracellular DNA (eDNA) is crucial for M. avium's environmental persistence and biofilm formation.
Purpose of the Study:
- To investigate the role of M. avium eDNA in macrophage survival and host immune response.
- To understand how M. avium eDNA influences pro-inflammatory cytokine production.
Main Methods:
- Utilized virulent M. avium strains and eDNA-deficient mutants.
- Compared responses with nonvirulent Mycobacterium smegmatis.
- Assessed macrophage survival, IL-1β, NLRP3, and IFN-β production.
Main Results:
- eDNA-deficient M. avium mutants showed attenuated macrophage survival.
- Mutants yielded significantly higher IL-1β compared to wildtype.
- M. avium suppressed IL-1β and NLRP3, while triggering IFN-β in a DNA-dependent manner.
Conclusions:
- M. avium eDNA plays a significant role in modulating host macrophage responses.
- eDNA contributes to M. avium's ability to evade immune detection and killing.
- Targeting M. avium eDNA could be a strategy to enhance host defense against infection.
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