PNAS：额外获得的基因让特定细菌获得感染能力
生物谷报道：本周，有研究者宣布发现了鸟分枝杆菌（Mycobacterium avium）感染组织细胞或巨噬细胞，从而促使机体免疫系统妥协的机制。此项由俄勒冈州立大学的研究者主持的研究成果将会发表在本周的Proceedings of the National Academy of Sciences杂志上。参与研究的还有来自内布拉斯加大学的研究者。
鸟分枝杆菌是一类可引起严重肺部感染，并在肺气肿和AIDS病人体内广泛存在的细菌。据俄勒冈州立大学的生物医学教授Luiz E. Bermudez介绍，赋予此类细菌进入变形虫以及人体的关键因素，是通过进化从其他细菌那获得的遗传物质中的一个“岛”。
“如果没有这些额外获得的基因，此细菌感染环境中变形虫的效率将会非常低，变形虫就是此细菌在环境中的宿主，” Bermudez介绍说，“事实上，这个效率几乎等于零。但是一旦有了包含这个‘岛’的遗传物质，此细菌就发现了一条进驻细胞的路子，从而掌控细胞，而不再发生吞噬作用。”（援引生命经纬）
原始出处:
Published online before print June 19, 2007, 10.1073/pnas.0610746104
Identification of Mycobacterium avium pathogenicity island important for macrophage and amoeba infection
( uptake )
, , 
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Departments of *Biomedical Sciences, College of Veterinary Medicine, and ¶Microbiology, College of Science, and Environmental Health Sciences Center, Oregon State University, Corvallis, OR 97331; and Department of Veterinary and Biomedical Sciences, University of Nebraska, Lincoln, NE 68583-0905
Edited by E. Peter Greenberg, University of Washington School of Medicine, Seattle, WA, and approved May 17, 2007 (received for review December 4, 2006)
The ability to infect macrophages is a common characteristic shared among many mycobacterial species. Mycobacterium avium, Mycobacterium tuberculosis, and Mycobacterium kansasii enter macrophages, using the complement receptors CR1, CR3, CR4, and the mannose receptor. To identify M. avium genes and host cell pathways involved in the bacterial uptake by macrophages, we screened a M. avium transposon mutant library for the inability to enter macrophages. Uptake-impaired clones were selected. Sequence of six M. avium clones identified one gene involved in glycopeptidolipid biosynthesis, one gene encoding the conserved membrane protein homologue to the M. avium subsp. paratuberculosis MAP2446c gene and four others belonging to the same region of the chromosome. Analysis of the chromosome region revealed a pathogenicity island inserted between two tRNA sequences with 58% of G+C content versus 69% in the M. avium genome. The region is unique for M. avium and is not present in M. tuberculosis or M. paratuberculosis. Although the mutants did not differ from the WT bacterium regarding the binding to macrophage cell membrane, analysis of macrophage proteins after 1 h infection revealed a deficiency in the mutant to phosphorylate certain proteins on uptake. To understand M. avium interaction with two evolutionarily distinct hosts, the mutants were evaluated for Acanthamoeba castellanii invasion. The defect in the ability of the mutants to invade both cells was highly similar, suggesting that M. avium might have evolved mechanisms that are used to enter amoebas and human macrophages.
Fig. 4. Mycobacterium induced actin cytoskeleton rearrangements in U937
cells. Macrophages were infected with M. avium WT (A), 9C3 mutant (B), 9C3
complemented strain (C), M. smegmatis WT (D), or M. smegmatis containing
pLDPI-Reg2 (E) for 15 min and 1 h. Bacteria (red) were labeled with rhodamine
(Left; Texas red channel) and the actin (green) was visualized by fluoresceinphalloidin
staining (Right; FITC channel). Slides were analyzed by using a
DM400B coded fluorescent microscope (Leica, Wetzlar, Germany).
英文全文链接：
http://www.pnas.org/cgi/reprint/0610746104v2.pdf
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