scholarly journals Influenza A Virus Infection of Intestinal Epithelial Cells Enhances the Adhesion Ability of Crohn’s Disease Associated Escherichia coli Strains

PLoS ONE ◽  
2015 ◽  
Vol 10 (2) ◽  
pp. e0117005 ◽  
Author(s):  
Marta Aleandri ◽  
Maria Pia Conte ◽  
Giovanna Simonetti ◽  
Simona Panella ◽  
Ignacio Celestino ◽  
...  
2019 ◽  
Vol 61 (3) ◽  
pp. 395-398
Author(s):  
Christin Peteranderl ◽  
Irina Kuznetsova ◽  
Jessica Schulze ◽  
Martin Hardt ◽  
Emilia Lecuona ◽  
...  

2007 ◽  
Vol 189 (13) ◽  
pp. 4860-4871 ◽  
Author(s):  
Marie-Agnès Bringer ◽  
Nathalie Rolhion ◽  
Anne-Lise Glasser ◽  
Arlette Darfeuille-Michaud

ABSTRACT Adherent-invasive Escherichia coli (AIEC) isolated from Crohn's disease patients is able to adhere to and invade intestinal epithelial cells and to replicate in mature phagolysosomes within macrophages. Here, we show that the dsbA gene, encoding a periplasmic oxidoreductase, was required for AIEC strain LF82 to adhere to intestinal epithelial cells and to survive within macrophages. The LF82-ΔdsbA mutant did not express flagella and, probably as a consequence of this, did not express type 1 pili. The role of DsbA in adhesion is restricted to the loss of flagella and type 1 pili, as forced contact between bacteria and cells and induced expression of type 1 pili restored the wild-type phenotype. In contrast, the dsbA gene is essential for AIEC LF82 bacteria to survive within macrophages, irrespective of the loss of flagella and type 1 pilus expression, and the survival ability of LF82-ΔdsbA was as low as that of the nonpathogenic E. coli K-12, which was efficiently killed by macrophages. We also provide evidence that the dsbA gene is needed for LF82 bacteria to grow and survive in an acidic and nutrient-poor medium that partly mimics the harsh environment of the phagocytic vacuole. In addition, under such stress conditions dsbA transcription is highly up-regulated. Finally, the CpxRA signaling pathway does not play a role in regulation of dsbA expression in AIEC LF82 bacteria under conditions similar to those of mature phagolysosomes.


2018 ◽  
Vol 49 (1) ◽  
Author(s):  
Yuguang Fu ◽  
Jie Tong ◽  
Fandan Meng ◽  
Doris Hoeltig ◽  
Guangliang Liu ◽  
...  

2010 ◽  
Vol 285 (44) ◽  
pp. 34016-34026 ◽  
Author(s):  
Allen C. Bateman ◽  
Rositsa Karamanska ◽  
Marc G. Busch ◽  
Anne Dell ◽  
Christopher W. Olsen ◽  
...  

2010 ◽  
Vol 192 (7) ◽  
pp. 1832-1843 ◽  
Author(s):  
Sylvie Miquel ◽  
Laurent Claret ◽  
Richard Bonnet ◽  
Imen Dorboz ◽  
Nicolas Barnich ◽  
...  

ABSTRACT The interaction of Crohn's disease (CD)-associated adherent-invasive Escherichia coli (AIEC) strain LF82 with intestinal epithelial cells depends on surface appendages, such as type 1 pili and flagella. Histone-like proteins operate as global regulators to control the expression of these virulence factors. We evaluated the role of histone-like proteins in AIEC reference strain LF82 during infection of intestinal epithelial cells, Intestine-407, and observed that the fis mRNA level was decreased. The role of Fis in AIEC LF82 was determined by studying the phenotype of an LF82 fis::Km mutant. This was the first mutant of strain LF82 that has been described thus far that is unable to express flagellin but still able to produce type 1 pili. The cyclic-di-GMP pathway linking flagella and type 1 pilus expression is not involved in Fis-mediated regulation, and we identified in the present study Fis-binding sites located upstream of the fimE gene and in the intergenic region between fimB and nanC of the fim operon encoding type 1 pili. The major consequence of decreased Fis expression in AIEC bacteria in contact with host cells is a direct downregulation of fimE expression, leading to the preferential ON phase of the fimS element. Thus, by maintaining type 1 pilus expression, AIEC bacteria, which interact with the gut mucosa, have greater ability to colonize and to induce inflammation in CD patients.


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