Journal
MEDICAL GAS RESEARCH
Volume 2, Issue -, Pages -Publisher
MEDKNOW PUBLICATIONS & MEDIA PVT LTD
DOI: 10.1186/2045-9912-2-30
Keywords
Carbon monoxide; Heme oxygenase; Microbiology; Immunology; Mycobacterium tuberculosis; Microbial pathogenesis
Categories
Funding
- Disease Oriented Clinical Scholar's program at UT Southwestern
- NIH [R01 AI099439, 5T32AI007520]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI099439] Funding Source: NIH RePORTER
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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.
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