Toll-like receptor 2 controls mucosal inflammation by regulating epithelial barrier function.

By E. Cario, Guido Gerken, D. Podolsky. Gastroenterology, 2007

696 citations recorded by the source corpus.

Subfields: Immunology, Immunology and Allergy, Neurology

View Paper: https://www.semanticscholar.org/paper/f64757c704faee96f24272921c4637d44503e0e5

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Citations in the corpus

Farnesoid X receptor activation inhibits inflammation and preserves the intestinal barrier in inflammatory bowel disease (2011, methodology): “In vivo intestinal permeability assay Intestinal permeability was examined in mice after 7 days of DSS treatment or 48 h after the second TNBS administration, as described previously.(23) Results were normalised to WT mice, which did not receive any treatment (n1⁄43).”
Toll-like receptors and cancer (2009, background): “In the large intestine, even in the absence of overt infection or injury, TLR activation mediates proper epithelial barrier function by strengthening tight junctions and inducing cytoprotective factor”
Toll-like receptor signalling in the intestinal epithelium: how bacterial recognition shapes intestinal function (2010, background): “Systemic administration of flagellin and the TLR2 ligand tripalmitoyl- S -glyceryl cysteine-serine 4 -lysine (Pam3CSK4) protects against DSS-induced coliti”
The Microbiome in Infectious Disease and Inflammation (2012, positive): “signaling plays critical roles in the maintenance of the functional tight junction barrier integrity of the intestinal epithelial layer (68).”
Gut microbiota in health and disease. (2010, background): “Furthermore, signaling via TLR2, which in vivo is principally stimulated by microbial cell wall peptidoglycan, was shown to promote the integrity of the intestinal epithelium through maintenance of tight junctions and decreased apoptosis (38).”
Mucosal healing in inflammatory bowel diseases: a systematic review (2012, background): “Activation by TLR2 or TLR4 ligands protects against mucosal injury and colitis, suggesting that TLR signalling is a target for modulating colitis, potentially by regulating trefoil factor 3 expression and preventing IEC apoptosis.(51) 52 The TLR5 agonist flagellin potentially protects IECs from bact”