TLR4 and MD-2 are up-regulated in inflammatory bowel disease (IBD): Mechanisms for dysregulated LPS signaling

Apical TLR ligation of intestinal epithelial cells drives a Th1-polarized regulatory or inflammatory type effector response in vitro

“…Our co-culture model reveals a role for TLR4 ligation of HT-29 cells in driving inflammatory responses, characterized by enhanced TNF-␣ production coinciding with decreased numbers of regulatory T cells. A phenotypically similar response has been observed in Crohn's disease (Ricciardelli et al 2008;Abreu et al 2003). Furthermore, during episodes of infection or inflammation the production of IL-6 has been shown to suppress the development and activity of CD4 + CD25 + Foxp3 + regulatory T cells (Bettelli et al 2006).…”

The Functional Role of Fecal Microbiota Transplantation on Dextran Sulfate Sodium-Induced Colitis in Mice

“…The results suggested four different component of FMT reduced the expression of TLR2, TLR4, and TLR5 caused by DSS, and the transplantation of fecal suspension showed more potent effect than other three groups (Figures 4A–C). TLR4 can bind to pathogen-associated molecules, initiate intracellular signal transduction by medullary differentiation factor 88 (MyD88), and finally activate nuclear factor-κB (NF-κB), triggering a series of expression of inflammatory mediators and destroying the intestinal immune homeostasis eventually leads to the development of UC (Abreu et al, 2003; Bank et al, 2014; Choo et al, 2017). Therefore, we further examined the expression of key proteins in the TLR4-MyD88-TRAF6-NF-κB signaling pathway.…”