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The existing body of evidence does not offer adequate support for the direct implication of CRP in modulating the advancement of ulcerative colitis.<\/jats:p><jats:p><jats:bold>Methods<\/jats:bold>: Our study employed a rigorous mouse model. An ulcerative colitis mouse model was established by subjecting CRP\u2010deficient mice to dextran sulfate sodium (DSS) treatment. The phenotype of the mice, which encompassed parameters such as body weight, colon length, and spleen weight, was meticulously evaluated. Additionally, various physiological and biochemical indicators were assessed, including colon histopathology, expression levels of inflammatory factors, and staining of the intestinal mucus layer.<\/jats:p><jats:p><jats:bold>Results:<\/jats:bold> The absence of CRP did not significantly affect the phenotype, physiological characteristics, and biochemical indices in a mouse model of ulcerative colitis compared to mice with wild\u2010type CRP. Additionally, eliminating intestinal bacteria flora interference through antibiotic treatment revealed that mice lacking CRP did not demonstrate any notable variations in the ulcerative colitis model. Meanwhile, the survival rate of mice lacking CRP did not exhibit a statistically significant difference compared to wild\u2010type mice.<\/jats:p><jats:p><jats:bold>Conclusion:<\/jats:bold> The results of our study suggest that CRP may not directly mediate ulcerative colitis. Instead, it is more likely to be a bystander that is present alongside with elevated inflammatory factors. Further investigation is warranted to determine the precise role of CRP in humans, given the significant limitations associated with the use of mouse models.<\/jats:p>","DOI":"10.1155\/2024\/1386147","type":"journal-article","created":{"date-parts":[[2024,10,1]],"date-time":"2024-10-01T11:18:58Z","timestamp":1727781538000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["C\u2010Reactive Protein Is Not the Driver Factor in Ulcerative 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