生物谷報道：本周,，有研究者宣布發(fā)現(xiàn)了鳥分枝桿菌（Mycobacterium avium）感染組織細胞或巨噬細胞，從而促使機體免疫系統(tǒng)妥協(xié)的機制,。此項由俄勒岡州立大學的研究者主持的研究成果將會發(fā)表在本周的Proceedings of the National Academy of Sciences雜志上。參與研究的還有來自內布拉斯加大學的研究者,。
鳥分枝桿菌是一類可引起嚴重肺部感染,，并在肺氣腫和AIDS病人體內廣泛存在的細菌。據俄勒岡州立大學的生物醫(yī)學教授Luiz E. Bermudez介紹,，賦予此類細菌進入變形蟲以及人體的關鍵因素,，是通過進化從其他細菌那獲得的遺傳物質中的一個“島”。
“如果沒有這些額外獲得的基因,，此細菌感染環(huán)境中變形蟲的效率將會非常低,，變形蟲就是此細菌在環(huán)境中的宿主，” Bermudez介紹說,，“事實上,，這個效率幾乎等于零。但是一旦有了包含這個‘島’的遺傳物質,，此細菌就發(fā)現(xiàn)了一條進駐細胞的路子,，從而掌控細胞，而不再發(fā)生吞噬作用,。”（援引生命經緯）
原始出處:
Published online before print June 19, 2007, 10.1073/pnas.0610746104
Identification of Mycobacterium avium pathogenicity island important for macrophage and amoeba infection
( uptake )
Lia Danelishvili *, Martin Wu *, Bernadette Stang *, Melanie Harriff *, Stuart Cirillo , Jeffrey Cirillo , Robert Bildfell *, Brian Arbogast , and Luiz E. Bermudez *¶||
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).
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