Fig. 2: The mechanisms of microbe-host interplay affecting gastric carcinogenesis. | npj Biofilms and Microbiomes

Fig. 2: The mechanisms of microbe-host interplay affecting gastric carcinogenesis.

From: The dynamic oral–gastric microbial axis connects oral and gastric health: current evidence and disputes

Fig. 2

Persistent H. pylori infection induces gastric gland atrophy and subsequently suppresses endocrine activity. The Bacteroidales family S24-7 activates ILC-2 to produce IL-5, contributing to diminished H. pylori. S. anginosus stimulates the recruitment of neutrophils and monocytes to mediate epithelial dysplasia. Oral-associated microbes produce carcinogens such as lactate, LPS, nitrite, and acetaldehyde. L-Lactate assists H. pylori in resisting complement C4b. P. melaninogenica LPS synergistic with TCDA promotes gastric epithelial cell proliferation by activating the IL-6/JAK1/STAT3 pathway. Acetaldehyde causes DNA damage and mutation in epithelial cells. Suppressed bacterial arginine degradation provides arginine availability for tumor cell growth. The direct effects and indirect effects are shown by solid and dashed arrows, respectively. Created with BioRender.com.

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