Escherichia coli K12: An evolving opportunistic commensal gut microbe distorts barrier integrity in human intestinal cells

2019 ◽  
Vol 133 ◽  
pp. 103545 ◽  
Author(s):  
Mohd Iqbal Bhat ◽  
Kandukuri Sowmya ◽  
Suman Kapila ◽  
Rajeev Kapila
2015 ◽  
Vol 79 (4) ◽  
pp. 603-607 ◽  
Author(s):  
Giovanni V. Coppa ◽  
Bruna Facinelli ◽  
Gloria Magi ◽  
Emanuela Marini ◽  
Lucia Zampini ◽  
...  

2008 ◽  
Vol 41 (6) ◽  
pp. 594-599 ◽  
Author(s):  
Baichong Yang ◽  
Xuemei Zhang ◽  
Xiaolan Bao ◽  
Ying Lv ◽  
Jing Zhang ◽  
...  

2004 ◽  
Vol 72 (8) ◽  
pp. 4859-4863 ◽  
Author(s):  
Sylvie Hudault ◽  
O. Brad Spiller ◽  
B. Paul Morgan ◽  
Alain L. Servin

ABSTRACT Afa/Dr diffusely adhering Escherichia coli (DAEC) bacteria that are responsible for recurrent urinary tract and gastrointestinal infections recognized as a receptor the glycosylphosphatidylinositol (GPI)-anchored protein decay-accelerating factor (DAF; CD55) at the brush border of cultured human intestinal cells. Results show that Afa/Dr DAEC C1845 bacteria were poorly associated with the mucosa of the gastrointestinal tract of infected mice. We conducted experiments with Chinese hamster ovary (CHO) cells stably transfected with mouse (GPI or transmembrane forms), pig, or human CD55 or mouse Crry cDNAs or transfected with empty vector pDR2EF1α. Recombinant E. coli AAEC185 bacteria expressing Dr or F1845 adhesins bound strongly to CHO cells expressing human CD55 but not to the CHO cells expressing mouse (transmembrane and GPI anchored), rat, or pig CD55 or mouse Crry. Positive clustering of CD55 around Dr-positive bacteria was observed in human CD55-expressing CHO cells but not around the rarely adhering Dr-positive bacteria randomly distributed at the cell surface of CHO cells expressing mouse, rat, or pig CD55.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Cheng-Rung Huang ◽  
Cheng-Ju Kuo ◽  
Chih-Wen Huang ◽  
Yu-Ting Chen ◽  
Bang-Yu Liu ◽  
...  

AbstractEnterohemorrhagic Escherichia coli (EHEC) induces changes to the intestinal cell cytoskeleton and formation of attaching and effacing lesions, characterized by the effacement of microvilli and then formation of actin pedestals to which the bacteria are tightly attached. Here, we use a Caenorhabditis elegans model of EHEC infection to show that microvillar effacement is mediated by a signalling pathway including mitotic cyclin-dependent kinase 1 (CDK1) and diaphanous-related formin 1 (CYK1). Similar observations are also made using EHEC-infected human intestinal cells in vitro. Our results support the use of C. elegans as a host model for studying attaching and effacing lesions in vivo, and reveal that the CDK1-formin signal axis is necessary for EHEC-induced microvillar effacement.


1983 ◽  
Vol 39 (3) ◽  
pp. 1102-1106 ◽  
Author(s):  
C F Deneke ◽  
K McGowan ◽  
G M Thorne ◽  
S L Gorbach

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