Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026918 (Mycobacterium)
 52,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The lack of innovative therapies and the emergence of multi-drug-resistant pathogens emphasize the urgency of finding new approaches to fighting intracellular pathogens in general and Mycobacterium tuberculosis in particular, especially given the fact that tuberculosis is widely recognized as a major health problem worldwide. This review describes how host phagocytic cellular Coronin-1A gene epigenomics can be used to understand the subversive strategy adopted by M. tuberculosis to avoid encounter with the harsh environment within the phagocytic vacuole, and how it may provide a novel approach for the prevention and treatment of tuberculosis.
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PMID:Coronin-1A epigenomics governs mycobacterial persistence in tuberculosis. 1803 35

Mycobacterium leprae is an intracellular pathogen that survives within the phagosome of host macrophages. Several host factors are involved in producing tolerance, while others are responsible for killing the mycobacterium. Tryptophan aspartate-containing coat protein (TACO; also known as CORO1A or coronin-1) inhibits the phagosome maturation that allows intracellular parasitization. In addition, the Toll-like receptor (TLR) activates the innate immune response. Both CORO1A and TLR-2 co-localize on the phagosomal membrane in the dermal lesions of patients with lepromatous leprosy. Therefore, we hypothesized that CORO1A and TLR-2 might interact functionally. This hypothesis was tested by investigating the effect of CORO1A in TLR-2-mediated signalling and, inversely, the effect of TLR-2-mediated signalling on CORO1A expression. We found that CORO1A suppresses TLR-mediated signal activation in human macrophages, and that TLR2-mediated activation of the innate immune response resulted in suppression of CORO1A expression. However, M. leprae infection inhibited the TLR-2-mediated CORO1A suppression and nuclear factor-kappaB activation. These results suggest that the balance between TLR-2-mediated signalling and CORO1A expression will be key in determining the fate of M. leprae following infection.
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PMID:Tryptophan aspartate-containing coat protein (CORO1A) suppresses Toll-like receptor signalling in Mycobacterium leprae infection. 1943 3