Heat shock protein 60 of Helicobacter pylori induces inflammatory responses through the toll-like receptor-triggered pathway in cultured human gastric epithelial cells

Lipopolysaccharide in bacterial chronic infection: Insights from Helicobacter pylori lipopolysaccharide and lipid A

“…In general, since TLR2 recognizes bacterial lipoproteins, lipopeptides and lipoteichoic acids, the numerous putative lipoproteins encoded in the H. pylori genome represent candidate TLR2 ligands (Doig et al, 1999). An H. pylori heat shock protein (Hsp60) has been implicated in activation of TLR2 (Takenaka et al, 2004), but this protein has also been reported to induce interleukin-6 production by macrophages via a TLR2-independent mechanism (Gobert et al, 2004). Additionally, recognition of non-invasive H. pylori by epithelial cells has been shown to be mediated by Nod1, an intracellular pattern recognition molecule with specificity for peptidoglycan-derived muropeptides, which are delivered intracellularly by the type IV secretion systemencoding cag PAI (Viala et al, 2004).…”

Chlamydia trachomatis heat shock proteins 60 and 10 induce apoptosis in endocervical epithelial cells

“…Similarly, Kol et al [37] have shown that cHSP60 and human HSP60 activate vascular endothelium, smooth muscle and macrophages to produce proinflammatory cytokines, and that this process is mediated by NF-jB. In another study by Takenaka et al [38], it was reported that recombinant HSP60 of Helicobacter pylori induces inflammatory responses through TLR-mediated NF-jB in cultured human gastric epithelial cells. Our results also suggest the involvement of cHSPs in activation of the NF-jB signaling pathway and production of proinflammatory cytokines.…”

Toll-like receptor 2: An important immunomodulatory molecule during Helicobacter pylori infection

“…HP-HSP60 is a TLR2 ligand so that the HSP60-mediated NF-κB activation and IL-8 production in a human gastric epithelial cell line were inhibited using an antibody against TLR2 [95]. HP-HSP60 was found to promote the secretion of IL-8 in a human monocytic cell line through activation of signal regulated kinase (ERK) and mitogen activated protein (MAP) kinases [96].…”