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Medical Gas Research

, 2:30

CO in biology and medicine

Abstract

The intracellular pathogen Mycobacterium tuberculosis Mtb is exposed to multiple host antimicrobial pathways, including toxic gases such as superoxide, nitric oxide and carbon monoxide CO. To survive, mycobacteria evolved mechanisms to resist the toxic environment, and in this review we focus on a relatively new field, namely, the role of macrophage heme oxygenase and its enzymatic product CO in Mtb pathogenesis. In particular, we focus on i the induction of heme oxygenase during Mtb infection and its relevance to Mtb pathogenesis, ii the ability of mycobacteria to catabolize CO, iii the transcriptional reprogramming of Mtb by exposure to CO, iv the general antimicrobial properties of CO and v new genetic evidence characterizing the ability of Mtb to resist CO toxicity. Developing a complete molecular and genetic understanding of the pathogenesis of Mtb is essential to its eventual eradication.

KeywordsCarbon monoxide Heme oxygenase Microbiology Immunology Mycobacterium tuberculosis Microbial pathogenesis AbbreviationsATPAdenosine triphosphate

COCarbon monoxide

CODHCarbon monoxide dehydrogenase

CORMCarbon monoxide releasing molecule

DNADeoxyribonucleic acid

dNTPDeoxyribonucleotide

H2O2Hydrogen peroxide

HOHeme oxygenase

IFN-βInterferon beta

IRF3Interferon regulatory factor 3

MtbMycobacterium tuberculosis

NONitric oxide

TNFTumor necrosis factor.

Electronic supplementary materialThe online version of this article doi:10.1186-2045-9912-2-30 contains supplementary material, which is available to authorized users.

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Autor: Vineetha M Zacharia - Michael U Shiloh

Fuente: https://link.springer.com/



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