jmm editor’s choice: how does helicobacter pylori cause inflammation?

posted on april 3, 2020   by 英格兰vs美国谁会赢？

the journal of medical microbiology (jmm) is a journal published by the 英格兰vs美国谁会赢？ , focused on providing comprehensive coverage of medical, dental and veterinary microbiology and infectious diseases, including bacteriology, virology, mycology and parasitology. this month, professor arunaloke chakrabarti discusses the paper ‘n-terminal region of helicobacter pylori caga induces il-8 production in gastric epithelial cells via the β1 integrin receptor’, which was selected as editor’s choice from the march issue of jmm.

“multiple epidemiological studies have shown a strong association of helicobacter pylori with gastric cancer. however, the pathogenesis of gastric cancer induced by h. pylori cytotoxin-associated antigen (caga) is not currently understood, though it remains of interest to many scientists in this field. from whole genome sequencing, interleukin-8 (il-8) was found to be the single most upregulated gene in h. pylori exposed to gastric epithelium.

previously, many researchers have focused on the role of the c-terminal domain of cytotoxin-associated antigen a (caga) in il-8 production. however, the authors in the present study evaluated the n-terminal region of caga and focused on 303-456 residues, as they interact with integrin b1 (itgb1). they showed that 303-456 residues of the n-terminal portion of extracellular caga can induce il-8 production by activating p38 through itgb1 or mapk erk1/2 signal pathway. though the authors acknowledge the present result is still not sufficient for the evidence of extracellular caga-induced il8 secretion, this is an important step in understanding pathogenesis of gastric cancer.”

n-terminal region of helicobacter pylori caga induces il-8 production in gastric epithelial cells via the β1 integrin receptor

helicobacter pylori is associated with gastrointestinal disease, most notably gastric cancer. cytotoxin-associated antigen a (caga) is an important virulence factor for h. pylori and causes host cells to release inflammatory factors, particularly interleukin-8 (il-8). the mechanism by which c-terminal caga induces il-8 production has been studied extensively, but little is known about the role of the n-terminus.

we investigated the effect of a peptide in the n-terminal of caga called caga_303–456aa on il-8 production by gastric epithelial cells, and showed that residues 303–456 of the n-terminal region of caga induce il-8 production via a caga_303-456–itgb1–p38–il-8 pathway.