The Gli1‐Snail axis contributes to Salmonella Typhimurium‐induced disruption of intercellular junctions of intestinal epithelial cells

2020 ◽  
Vol 22 (8) ◽  
Author(s):  
Wei Liu ◽  
Tao Ruan ◽  
Xiaoyue Ji ◽  
Di Ran ◽  
Jing Sun ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Salmonella Typhimurium ◽  
Intestinal Epithelial Cells ◽  
Intercellular Junctions ◽  
Intestinal Epithelial

scholarly journals Evaluation of Novel Probiotic Bacillus Strains Based on Enzyme Production and Protective Activity Against Salmonellosis

2019 ◽  
Vol 69 (4) ◽  
pp. 1205
Author(s):  
Nazila Ghorban Hosseini ◽  
Mohammad Hossein Modarressi ◽  
Seyed Naser Mousavi ◽  
Maryam Tajabadi Ebrahimi
Keyword(s):  
Epithelial Cells ◽  
Salmonella Typhimurium ◽  
Intestinal Epithelial Cells ◽  
Bacillus Species ◽  
Poultry Production ◽  
Intestinal Epithelial ◽  
Salmonella Spp ◽  
Bacillus Tequilensis ◽  
Bacillus Spp ◽  
North Of Iran

Probiotic strains of Bacillus Species are used in industrial poultry production because of their ability to produce enzymes enhancing the absorption of food, and their ability to reduce the risk of Salmonella spp. infection. The aim of this study was to isolate native potential probiotic Bacillus spp. with the ability to produce enzymes and attachment to intestinal epithelial cells in order to prevent Salmonella typhimurium infection. First, 25 samples of chicken feces were collected from 7 industrial poultry in Golestan province located in north of Iran. Bacillus species from samples were isolated on nutrient agar. These strains were evaluated for the ability of producing amyalse and phytase and their probiotic characteristics such as bile salt, acid and antibiotic resistance, the ability to attach to intestinal epithelial cells and inhibit Salmonella typhimurium invasion. Then selected isolates were identified based on 16S rDNA.  Results showed that from 86 isolated, 4 Bacillus strains‌ had desirable characteristics such as the ability to produce phytase and amylase and having suitable probiotics features. We identified K03, K02, and K20 isolates as Bacillus tequilensis and K20 as Bacillus subtilis. Bacillus tequilensis K03 showed the highest attachment ability to intestinal epithelium cells and could inhibited Salmonella typhimurium attachment.

scholarly journals Apical Invasion of Intestinal Epithelial Cells by Salmonella typhimurium Requires Villin to Remodel the Brush Border Actin Cytoskeleton

2015 ◽  
Vol 17 (2) ◽  
pp. 164-177 ◽  
Author(s):  
Nouara Lhocine ◽  
Ellen T. Arena ◽  
Perrine Bomme ◽  
Florent Ubelmann ◽  
Marie-Christine Prévost ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Actin Cytoskeleton ◽  
Salmonella Typhimurium ◽  
Brush Border ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

scholarly journals Orchestration of Neutrophil Movement by Intestinal Epithelial Cells in Response to Salmonella typhimurium Can Be Uncoupled from Bacterial Internalization

1999 ◽  
Vol 67 (2) ◽  
pp. 608-617 ◽  
Author(s):  
Andrew T. Gewirtz ◽  
Andrew M. Siber ◽  
James L. Madara ◽  
Beth A. McCormick
Keyword(s):  
Epithelial Cells ◽  
Salmonella Typhimurium ◽  
Signaling Pathways ◽  
Intestinal Epithelial Cells ◽  
Intestinal Lumen ◽  
Bacterial Invasion ◽  
Apical Surface ◽  
Intestinal Epithelial ◽  
Membrane Ruffling ◽  
Intestinal Epithelia

ABSTRACT Intestinal epithelial cells respond to Salmonella typhimurium by internalizing this pathogen and secreting, in a polarized manner, an array of chemokines which direct polymorphonuclear leukocyte (PMN) movement. Notably, interleukin-8 (IL-8) is secreted basolaterally and directs PMN through the lamina propria, whereas pathogen-elicited epithelial chemoattractant (PEEC) is secreted apically and directs PMN migration across the epithelial monolayer to the intestinal lumen. While most studies of S. typhimuriumpathogenicity have focused on the mechanism by which this bacterium invades its host, the enteritis characteristically associated with salmonellosis appears to be more directly attributable to the PMN movement that occurs in response to this pathogen. Therefore, we sought to better understand the relationship between S. typhimurium invasion and epithelial promotion of PMN movement. First, we investigated whether S. typhimurium becoming intracellular was necessary or sufficient to induce epithelial promotion of PMN movement. Blocking S. typhimurium invasion by preventing, with cytochalasin D, the epithelial cytoskeletal rearrangements which mediate internalization did not reduce the epithelial promotion of PMN movement. Conversely, bacterial attainment of an intracellular position was not sufficient to induce model epithelia to direct PMN transmigration, since neither basolateral invasion by S. typhimurium nor apical internalization of an invasion-deficient mutant (achieved by inducing membrane ruffling with epidermal growth factor) induced this epithelial cell response. These results indicate that specific interactions between the apical surface of epithelial cells and S. typhimurium, rather than simply bacterial invasion, mediate the epithelial direction of PMN transmigration. To further investigate the means by which S. typhimurium induces epithelia to direct PMN movement, we investigated whether the same signaling pathways regulate secretion of IL-8 and PEEC. IL-8 secretion, but not PEEC secretion, was activated by phorbol myristate acetate and blocked by an inhibitor (mg-132) of the proteosome which mediates NF-κβ activation. Further, secretion of IL-8, but not PEEC, was activated by an entry-deficient (HilΔ)S. typhimurium mutant or by basolateral invasion of a wild-type strain. Together, these results indicate that distinct signaling pathways mediate S. typhimurium invasion, induction of IL-8 secretion, and induction of PEEC secretion in model intestinal epithelia.

scholarly journals Salmonella typhimurium infection increases p53 acetylation in intestinal epithelial cells

2010 ◽  
Vol 298 (5) ◽  
pp. G784-G794 ◽  
Author(s):  
Shaoping Wu ◽  
Zhongde Ye ◽  
Xingyin Liu ◽  
Yun Zhao ◽  
Yinglin Xia ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Salmonella Typhimurium ◽  
Inflammatory Responses ◽  
Intestinal Epithelial Cells ◽  
Secretion System ◽  
Intestinal Epithelial ◽  
Salmonella Infection ◽  
P53 Pathway ◽  
Type Three Secretion System ◽  
Type Three Secretion

The ability of Salmonella typhimurium to enter intestinal epithelial cells constitutes a crucial step in pathogenesis. Salmonella invasion of the intestinal epithelium requires bacterial type three secretion system. Type three secretion system is a transport device that injects virulence proteins, called effectors, to paralyze or reprogram the eukaryotic cells. Avirulence factor for Salmonella (AvrA) is a Salmonella effector that inhibits the host's inflammatory responses. The mechanism by which AvrA modulates host cell signaling is not entirely clear. p53 is situated at the crossroads of a network of signaling pathways that are essential for genotoxic and nongenotoxic stress responses. We hypothesized that Salmonella infection activates the p53 pathway. We demonstrated that Salmonella infection increased p53 acetylation. Cells infected with AvrA-sufficient Salmonella have increased p53 acetylation, whereas cells infected with AvrA-deficient Salmonella have less p53 acetylation. In a cell-free system, AvrA possessed acetyltransferase activity and used p53 as a substrate. AvrA expression increased p53 transcriptional activity and induced cell cycle arrest. HCT116 p53−/− cells had less inflammatory responses. In a mouse model of Salmonella infection, intestinal epithelial p53 acetylation was increased by AvrA expression. Our studies provide novel mechanistic evidence that Salmonella modulates the p53 pathway during intestinal inflammation and infection.

Pten gene deletion in intestinal epithelial cells enhances susceptibility to Salmonella Typhimurium infection in mice

2019 ◽  
Vol 57 (11) ◽  
pp. 1012-1018 ◽  
Author(s):  
Cody Howe ◽  
Jonathon Mitchell ◽  
Su Jin Kim ◽  
Eunok Im ◽  
Sang Hoon Rhee
Keyword(s):  
Epithelial Cells ◽  
Salmonella Typhimurium ◽  
Gene Deletion ◽  
Intestinal Epithelial Cells ◽  
Pten Gene ◽  
Intestinal Epithelial
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