{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T14:07:45Z","timestamp":1788876465160,"version":"build-2803163510"},"reference-count":202,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T00:00:00Z","timestamp":1788825600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Persistent colonization by gastrointestinal pathogens is an important environmental factor contributing to the development and progression of gastric and colorectal cancer.\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    (\n                    <jats:italic>H. pylori<\/jats:italic>\n                    ), Epstein-Barr virus (EBV),\n                    <jats:italic>Fusobacterium nucleatum<\/jats:italic>\n                    (\n                    <jats:italic>F. nucleatum<\/jats:italic>\n                    ), enterotoxigenic\n                    <jats:italic>Bacteroides fragilis<\/jats:italic>\n                    (ETBF), and pks-positive\n                    <jats:italic>Escherichia coli<\/jats:italic>\n                    (\n                    <jats:italic>E. coli<\/jats:italic>\n                    ) can induce chronic inflammation and reshape the tumor microenvironment via virulence factors, epithelial barrier disruption, DNA damage, and immune dysregulation. Conventional views have largely focused on the tumor-promoting effects of chronic inflammation; however, this view does not fully explain the coexsistence of persistent inflammation and immune evasion during chronic infection. In this review, we proposed that the key feature of pathogen-associated inflammation is not simply its intensity but rather the imbalance between sustained inflammatory stimulation and insufficient immune elimination. Rather than treating pathogen-mediated immune evasion, host-derived innate immune negative regulation, and adaptive immune checkpoint suppression as parallel mechanisms, this review examined how these functionally distinct layers converge in gastrointestinal tumors. Pathogen immune evasion allows persistent microbial stimulation, host negative-feedback pathways dampen PRR- and interferon (IFN)-associated signaling, and checkpoint-mediated suppression further impairs cytotoxic clearance. Together, these processes create a state in which sustained inflammation coexists with insufficient immune elimination. This state can impair antigen presentation, cytotoxic immune responses, and pathogen clearance, thereby promoting immune tolerance and tumor progression. Understanding this mechanism may offer a conceptual basis for pathogen control, innate immune reprogramming, and precision therapeutic intervention in gastrointestinal tumors.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1951036","type":"journal-article","created":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T13:14:40Z","timestamp":1788873280000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Interplay between pathogen-mediated immune evasion and innate immune negative regulation in gastrointestinal tumors"],"prefix":"10.3389","volume":"17","author":[{"given":"Mengxi","family":"Shi","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, Sichuan Provincial People\u2019s Hospital, University of Electronic Science and Technology of China","place":["Chengdu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yihua","family":"Zeng","sequence":"additional","affiliation":[{"name":"Department of Respiratory and Critical Care Medicine, West China Hospital, Sichuan University\/West China School of Nursing, Sichuan University","place":["Chengdu, Sichuan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chao","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Thyroid Surgery, Sichuan Provincial People\u2019s Hospital, University of Electronic Science and Technology of China","place":["Chengdu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaofei","family":"Zuo","sequence":"additional","affiliation":[{"name":"Department of Gastrointestinal Surgery, Sichuan Provincial People\u2019s Hospital, University of Electronic Science and Technology of China","place":["Chengdu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,8]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"17036","DOI":"10.1038\/nrdp.2017.36","article-title":"Gastric adenocarcinoma","volume":"3","author":"Ajani","year":"2017","journal-title":"Nat Rev Dis Primers"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cgh.2019.07.045","article-title":"Burden of gastric cancer","volume":"18","author":"Thrift","year":"2020","journal-title":"Clin Gastroenterol Hepatol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.3322\/caac.21834","article-title":"Global cancer statistics 2022: Globocan estimates of incidence and mortality worldwide for 36 cancers in 185 countries","volume":"74","author":"Bray","year":"2024","journal-title":"CA Cancer J Clin"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/s0140-6736(20)31288-5","article-title":"Gastric 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