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侵袭性作为一些具有不同罕见紧密黏附素类型的非典型肠致病性大肠杆菌菌株的一种假定的额外毒力机制。

Invasiveness as a putative additional virulence mechanism of some atypical Enteropathogenic Escherichia coli strains with different uncommon intimin types.

作者信息

Yamamoto Denise, Hernandes Rodrigo T, Blanco Miguel, Greune Lilo, Schmidt M Alexander, Carneiro Sylvia M, Dahbi Ghizlane, Blanco Jesús E, Mora Azucena, Blanco Jorge, Gomes Tânia A T

机构信息

Universidade Federal de São Paulo, Rua Botucatu, 862, 3o andar, Vila Clementino, São Paulo, CEP 04023-062, Brazil.

出版信息

BMC Microbiol. 2009 Jul 21;9:146. doi: 10.1186/1471-2180-9-146.

Abstract

BACKGROUND

Enteropathogenic Escherichia coli (EPEC) produce attaching/effacing (A/E) lesions on eukaryotic cells mediated by the outer membrane adhesin intimin. EPEC are sub-grouped into typical (tEPEC) and atypical (aEPEC). We have recently demonstrated that aEPEC strain 1551-2 (serotype O non-typable, non-motile) invades HeLa cells by a process dependent on the expression of intimin sub-type omicron. In this study, we evaluated whether aEPEC strains expressing other intimin sub-types are also invasive using the quantitative gentamicin protection assay. We also evaluated whether aEPEC invade differentiated intestinal T84 cells.

RESULTS

Five of six strains invaded HeLa and T84 cells in a range of 13.3%-20.9% and 5.8%-17.8%, respectively, of the total cell-associated bacteria. The strains studied were significantly more invasive than prototype tEPEC strain E2348/69 (1.4% and 0.5% in HeLa and T84 cells, respectively). Invasiveness was confirmed by transmission electron microscopy. We also showed that invasion of HeLa cells by aEPEC 1551-2 depended on actin filaments, but not on microtubules. In addition, disruption of tight junctions enhanced its invasion efficiency in T84 cells, suggesting preferential invasion via a non-differentiated surface.

CONCLUSION

Some aEPEC strains may invade intestinal cells in vitro with varying efficiencies and independently of the intimin sub-type.

摘要

背景

肠致病性大肠杆菌(EPEC)通过外膜黏附素紧密黏附素介导,在真核细胞上产生黏附/抹消(A/E)损伤。EPEC可分为典型(tEPEC)和非典型(aEPEC)两类。我们最近证明,aEPEC菌株1551-2(血清型O不可分型、无动力)通过依赖于紧密黏附素亚型omicron表达的过程侵入HeLa细胞。在本研究中,我们使用定量庆大霉素保护试验评估表达其他紧密黏附素亚型的aEPEC菌株是否也具有侵袭性。我们还评估了aEPEC是否侵入分化的肠道T84细胞。

结果

六株菌株中有五株分别以占总细胞相关细菌的13.3%-20.9%和5.8%-17.8%的比例侵入HeLa细胞和T84细胞。所研究的菌株比原型tEPEC菌株E2348/69的侵袭性显著更高(在HeLa细胞和T84细胞中分别为1.4%和0.5%)。通过透射电子显微镜证实了侵袭性。我们还表明,aEPEC 1551-2对HeLa细胞的侵袭依赖于肌动蛋白丝,但不依赖于微管。此外,紧密连接的破坏增强了其在T84细胞中的侵袭效率,表明通过未分化表面的优先侵袭。

结论

一些aEPEC菌株可能在体外以不同效率侵入肠道细胞,且与紧密黏附素亚型无关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e638/2724384/309411192862/1471-2180-9-146-1.jpg

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