小肠表皮在有细菌感染时迅速自我更新，并从基膜脱落，这个过程起针对病原体的一个防卫体系的作用。尽管如此，很多肠道病原体细菌也能在小肠表皮上生存。
现在，一个使病原体能够克服这种形式的宿主防卫的机制已被发现。Shigella毒性因子OspE（也见于很多其他肠道病原体细菌）可通过跟与整合蛋白连接在一起的激酶发生相互作用来增强宿主-细胞-基质粘合力。这样可能会抑制表皮脱落，帮助细菌在小肠表皮内形成菌落。这表明，能够阻断毒性因子OspE对与整合蛋白连接在一起的激酶之“劫持”的小分子也许对某些类型的小肠细菌感染有疗效。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature 459, 578-582 (28 May 2009) | doi:10.1038/nature07952
Bacteria hijack integrin-linked kinase to stabilize focal adhesions and block cell detachment
Minsoo Kim1,3, Michinaga Ogawa2,3, Yukihiro Fujita2,3, Yuko Yoshikawa2,3, Takeshi Nagai2,3, Tomohiro Koyama4, Shinya Nagai4, Anika Lange5, Reinhard F?ssler5 & Chihiro Sasakawa1,2,3
1 Department of Infectious Disease Control, International Research Center for Infectious Diseases,
2 Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan
3 CREST, Japan Science and Technology Agency, Kawaguchi 332-0012, Japan
4 Nippon Institute for Biological Science, 9-2221-1, Shinmachi, Ome, Tokyo 198-0024, Japan
5 Department of Molecular Medicine, Max-Planck Institute of Biochemistry, D-82152, Martinsried, Germany
The rapid turnover and exfoliation of mucosal epithelial cells provides an innate defence system against bacterial infection1, 2. Nevertheless, many pathogenic bacteria, including Shigella, are able to surmount exfoliation and colonize the epithelium efficiently3, 4. Here we show that the Shigella flexneri effector OspE5, 6 (consisting of OspE1 and OspE2 proteins), which is highly conserved among enteropathogenic Escherichia coli, enterohaemorrhagic E. coli, Citrobacter rodentium and Salmonella strains7, reinforces host cell adherence to the basement membrane by interacting with integrin-linked kinase (ILK)8. The number of focal adhesions was augmented along with membrane fraction ILK by ILK–OspE binding. The interaction between ILK and OspE increased cell surface levels of 1 integrin and suppressed phosphorylation of focal adhesion kinase and paxillin, which are required for rapid turnover of focal adhesion in cell motility9. Nocodazole-washout-induced focal adhesion disassembly was blocked by expression of OspE. Polarized epithelial cells infected with a Shigella mutant lacking the ospE gene underwent more rapid cell detachment than cells infected with wild-type Shigella. Infection of guinea pig colons with Shigella corroborated the pivotal role of the OspE–ILK interaction in suppressing epithelial detachment, increasing bacterial cell-to-cell spreading, and promoting bacterial colonization. These results indicate that Shigella sustain their infectious foothold by using special tactics to prevent detachment of infected cells.
