Open AccessHelicobacter pylori infection reduces TAMs infiltration in a mouse model of AOM/DSS induced colitis-associated cancer
Author(s) -
Luo-na Li,
Yun Liu,
Hong-chen Zhang,
Ting Wu,
Yun Dai,
Weihong Wang
Publication year - 2020
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0241840
Subject(s) - azoxymethane , colitis , inflammatory bowel disease , helicobacter pylori , infiltration (hvac) , medicine , helicobacter pylori infection , tumor necrosis factor alpha , colorectal cancer , proinflammatory cytokine , immunology , cancer research , cancer , inflammation , disease , gastroenterology , physics , thermodynamics
Inflammatory bowel disease (IBD) increases the risk of colitis-associated cancer (CAC). Evidences suggest that Helicobacter pylori ( H . pylori ) infection is associated with a low risk of IBD and protects against experimental colitis in mouse models. However, the effect of H . pylori infection in CAC remains unclear. We previously reported that H . pylori infection increased M2 macrophages in dextran sodium sulfate (DSS)-induced chronic colitis. Tumor-associated macrophages (TAMs) play a pivotal role in colon cancer. Therefore, we established a H . pylori -infected CAC mouse model induced by azoxymethane and DSS to explore the effect of H . pylori infection on TAMs in CAC. Here, we demonstrated that H . pylori infection attenuated the development of CAC by decreasing tumor multiplicity, tumor size, tumor grade and colitis scores. Moreover, H . pylori infection reduced the infiltration of TAMs, particularly M2-like TAMs in CAC tumors, accompanied with the down-regulated pro-inflammatory and pro-tumorigenic factors TNF-α, IL-1β, IL-6 and IL-23 in tumors of CAC mice. Our study suggests that H . pylori infection can reduce TAMs infiltration and regulate cytokines expression in CAC.