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1

Mechanisms of Mycobacterium avium pathogenesis

100%
Bermudez L. E., Wagner D., Sosnowska D.
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vol. 48
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issue 5
521-528
EN
Infections caused by M. avium are common in AIDS patients and patients with chronic lung diseases. The bacterium can be acquired both by the intestinal route and respiratory route. M. avium is capable of invading mucosal epithelial cells and translocate across the mucosa. The bacterium can infect macrophages interfering with several functions of the host cell. The host defense against M. avium is primarily dependent on CD4+ T lymphocytes and NK cells. Activated macrophages can inhibit or kill intracellular bacteria by mechanisms that are currently unknown but M. avium can invade resting macrophages and suppress key aspects of its function by triggering the release of TGF-beta and IL-10. Co-infection with HIV-1 appears to be mutually beneficial with both organisms growing faster.
2

Prospects for development of new antimycobacterial drugs, with special reference to a new benzoxazinorifamycin, KRM-1648

70%
Tomioka H.
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vol. 48
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issue 3
183-188
EN
In this article, I have thoroughly reviewed the status of development of new antimycobacterial drugs, in particular, rifamycin derivatives (rifabutin, rifapentine, and a new benzoxazinorifamycin, KRM-1648), fluoroquinolones (ciprofloxacin, ofloxacin, sparfloxacin, levofloxacin, gatifloxacin, sitafloxacin, moxifloxacin, and others), new macrolides (clarithromycin, azithromycin, roxithromycin), and others. In this review, I have mainly described the in vitro and in vivo activities of these drugs against Mycobacterium tuberculosis and atypical mycobacteria, especially Mycobacterium avium complex. In addition, therapeutic efficacy of these drugs in cases of clinical treatment of mycobacterial infections have also been briefly mentioned.
3

Abnormalities in the handling of intracellular bacteria in Crohn's disease: a link between infectious etiology and host genetic susceptibility

70%
Glasser A.-L., Darfeuille-Michaud A.
Archivum Immunologiae et Therapiae Experimentalis
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2008
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vol. 56
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issue 4
237-244
EN
The etiology of Crohn's disease (CD) is still poorly understood, but recent advances have highlighted the importance of the innate immune system and the critical relationship between the gut flora and the intestinal mucosa. Several combinations of genetic factors predisposing to CD have been described, with the most significant replicable associations including genes for intracellular receptors of bacterial cell walls (NOD2/CARD15) and for bacterial clearance and antigen processing via autophagy (ATG16L1 and IRGM). One theoretical link between susceptibility genes NOD2/CARD15, ATG16L1, and IRGM is that CD is primarily induced by the presence of a dysfunctional immunological response to persistent infection by intracellular bacterial pathogens such as Mycobacterium avium subspecies paratuberculosis or adherent-invasive Escherichia coli, both first-rank candidates on the basis of host genetic susceptibility, which concerns impaired functions in the defense against intracellular bacteria.
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