Mutation in alkylhydroperoxidase D gene dramatically decreases persistence of &lt;i&gt;Mycobacterium bovis&lt;/i&gt; bacillus calmette-guerin in infected macrophage

Farivar, Taghi Naserpour; Varnousfaderani, Pouran Johari; Borji, Abasalt

doi:10.4103/0019-5359.42023

Cited by 2 publications

(1 citation statement)

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“…Mtb strains harboring inactive mutants of components of the AhpC complex are susceptible to killing by murine macrophages expressing acidified nitrite and iNOS (Shi and Ehrt, 2006; Maksymiuk et al, 2015), underscoring the importance of this enzyme for detoxification of reactive nitrogen species by Mtb . Moreover, the persistence of Mycobacterium bovis bacillus Calmette-Guerin in infected macrophages decreases when bacterial AhpD is inactivated (Farivar et al, 2008). Mtb strains lacking AhpC show increased susceptibility to ROOH (Springer et al, 2001) and peroxynitrite, and decreased survival in macrophages (Master et al, 2002).…”

Section: Pathogen Virulence and Antioxidant Networkmentioning

confidence: 99%

Reactive species and pathogen antioxidant networks during phagocytosis

Piacenza

Trujillo

Radí

2019

Journal of Experimental Medicine

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The generation of phagosomal cytotoxic reactive species (i.e., free radicals and oxidants) by activated macrophages and neutrophils is a crucial process for the control of intracellular pathogens. The chemical nature of these species, the reactions they are involved in, and the subsequent effects are multifaceted and depend on several host- and pathogen-derived factors that influence their production rates and catabolism inside the phagosome. Pathogens rely on an intricate and synergistic antioxidant armamentarium that ensures their own survival by detoxifying reactive species. In this review, we discuss the generation, kinetics, and toxicity of reactive species generated in phagocytes, with a focus on the response of macrophages to internalized pathogens and concentrating on Mycobacterium tuberculosis and Trypanosoma cruzi as examples of bacterial and parasitic infection, respectively. The ability of pathogens to deal with host-derived reactive species largely depends on the competence of their antioxidant networks at the onset of invasion, which in turn can tilt the balance toward pathogen survival, proliferation, and virulence over redox-dependent control of infection.

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