scholarly journals WD40 Repeat Protein 26 Negatively Regulates Formyl Peptide Receptor-1 Mediated Wound Healing in Intestinal Epithelial Cells

2020 ◽  
Vol 190 (10) ◽  
pp. 2029-2038
Author(s):  
Mizuho Hasegawa ◽  
Charles A. Parkos ◽  
Asma Nusrat
Keyword(s):  
Wound Healing ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Formyl Peptide Receptor ◽  
Intestinal Epithelial ◽  
Wd40 Repeat ◽  
Repeat Protein ◽  
Peptide Receptor ◽  
Formyl Peptide

scholarly journals N‐formyl peptide receptor‐1 is important for homeostasis of intestinal epithelial cells

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Ashfaqul Alam ◽  
Giovanna Leoni ◽  
Christy Wentworth ◽  
Asma Nusrat ◽  
Andrew Neish
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Formyl Peptide Receptor ◽  
Intestinal Epithelial ◽  
Peptide Receptor ◽  
Formyl Peptide

scholarly journals Salmonella typhimurium attachment to human intestinal epithelial monolayers: transcellular signalling to subepithelial neutrophils.

1993 ◽  
Vol 123 (4) ◽  
pp. 895-907 ◽  
Author(s):  
B A McCormick ◽  
S P Colgan ◽  
C Delp-Archer ◽  
S I Miller ◽  
J L Madara
Keyword(s):  
Epithelial Cells ◽  
Salmonella Typhimurium ◽  
Apical Membrane ◽  
Coli Strain ◽  
Formyl Peptide Receptor ◽  
Human Neutrophils ◽  
Classical Pathway ◽  
Intestinal Epithelial ◽  
Formyl Peptide

In human intestinal disease induced by Salmonella typhimurium, transepithelial migration of neutrophils (PMN) rapidly follows attachment of the bacteria to the epithelial apical membrane. In this report, we model those interactions in vitro, using polarized monolayers of the human intestinal epithelial cell, T84, isolated human PMN, and S. typhimurium. We show that Salmonella attachment to T84 cell apical membranes did not alter monolayer integrity as assessed by transepithelial resistance and measurements of ion transport. However, when human neutrophils were subsequently placed on the basolateral surface of monolayers apically colonized by Salmonella, physiologically directed transepithelial PMN migration ensued. In contrast, attachment of a non-pathogenic Escherichia coli strain to the apical membrane of epithelial cells at comparable densities failed to stimulate a directed PMN transepithelial migration. Use of the n-formyl-peptide receptor antagonist N-t-BOC-1-methionyl-1-leucyl-1- phenylalanine (tBOC-MLP) indicated that the Salmonella-induced PMN transepithelial migration response was not attributable to the classical pathway by which bacteria induce directed migration of PMN. Moreover, the PMN transmigration response required Salmonella adhesion to the epithelial apical membrane and subsequent reciprocal protein synthesis in both bacteria and epithelial cells. Among the events stimulated by this interaction was the epithelial synthesis and polarized release of the potent PMN chemotactic peptide interleukin-8 (IL-8). However, IL-8 neutralization, transfer, and induction experiments indicated that this cytokine was not responsible for the elicited PMN transmigration. These data indicate that a novel transcellular pathway exists in which subepithelial PMN respond to lumenal pathogens across a functionally intact epithelium. Based on the known unique characteristics of the intestinal mucosa, we speculate that IL-8 may act in concert with an as yet unidentified transcellular chemotactic factor(s) (TCF) which directs PMN migration across the intestinal epithelium.

Tu1865 IL-28 Signaling in Intestinal Epithelial Cells Leads to a Revised Mucosal Wound Healing

2012 ◽  
Vol 142 (5) ◽  
pp. S-864
Author(s):  
Heike Dornhoff ◽  
Konstantin Fietkau ◽  
Sean Doyle ◽  
Markus F. Neurath ◽  
Jürgen Siebler
Keyword(s):  
Wound Healing ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Mucosal Wound

W1600 STAT3 Links IL-22 Signalling in Intestinal Epithelial Cells to Mucosal Wound Healing

2009 ◽  
Vol 136 (5) ◽  
pp. A-700
Author(s):  
Geethanjali Pickert ◽  
Clemens Neufert ◽  
Moritz Leppkes ◽  
Alexei Nikolaev ◽  
Hans-Anton Lehr ◽  
...  
Keyword(s):  
Wound Healing ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Mucosal Wound

scholarly journals STAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healing

2009 ◽  
Vol 206 (7) ◽  
pp. 1465-1472 ◽  
Author(s):  
Geethanjali Pickert ◽  
Clemens Neufert ◽  
Moritz Leppkes ◽  
Yan Zheng ◽  
Nadine Wittkopf ◽  
...  
Keyword(s):  
Wound Healing ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Genetically Engineered ◽  
Conditional Knockout ◽  
Cellular Stress Response ◽  
Cytokine Signaling ◽  
Intestinal Epithelial ◽  
Genetically Engineered Mice ◽  
Mucosal Wound

Signal transducer and activator of transcription (STAT) 3 is a pleiotropic transcription factor with important functions in cytokine signaling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. We demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IECs). Studies in genetically engineered mice showed that epithelial STAT3 activation in dextran sodium sulfate colitis is dependent on interleukin (IL)-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC-specific deletion of STAT3 activity were highly susceptible to experimental colitis, indicating that epithelial STAT3 regulates gut homeostasis. STAT3IEC-KO mice, upon induction of colitis, showed a striking defect of epithelial restitution. Gene chip analysis indicated that STAT3 regulates the cellular stress response, apoptosis, and pathways associated with wound healing in IECs. Consistently, both IL-22 and epithelial STAT3 were found to be important in wound-healing experiments in vivo. In summary, our data suggest that intestinal epithelial STAT3 activation regulates immune homeostasis in the gut by promoting IL-22–dependent mucosal wound healing.

Daikenchuto and ITS Bioactive Compartment, Ginsenoside RB1 Enhanced Wound Healing of Intestinal Epithelial Cells

2017 ◽  
Vol 152 (5) ◽  
pp. S969
Author(s):  
Yuki Toyokawa ◽  
Tomohisa Takagi ◽  
Kazuhiko Uchiyama ◽  
Saori Kashiwagi ◽  
Yuji Naito ◽  
...  
Keyword(s):  
Wound Healing ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Ginsenoside Rb1
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