{"title":"C-Reactive Protein Is Not the Driver Factor in Ulcerative Colitis.","authors":"Zhong-Bo Ge, Xin-Yun Zhang, Chun-Miao Zhang, Tao-Tao Xu, Si-Yi Li, Meng-Xiao Wei, Xin-Yuan Ding, Cai-Juan Bai, Han Wang, Hai-Hong Zhou, Ming-Yu Wang","doi":"10.1155/2024/1386147","DOIUrl":null,"url":null,"abstract":"<p><p><b>Purpose</b>: C-reactive protein (CRP) functions as a nonspecific marker in various inflammatory disorders, particularly in evaluating the efficacy of pharmacological treatments in patients with ulcerative colitis. The existing body of evidence does not offer adequate support for the direct implication of CRP in modulating the advancement of ulcerative colitis. <b>Methods</b>: Our study employed a rigorous mouse model. An ulcerative colitis mouse model was established by subjecting CRP-deficient 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. <b>Results:</b> 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-type 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-type mice. <b>Conclusion:</b> 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.</p>","PeriodicalId":12597,"journal":{"name":"Gastroenterology Research and Practice","volume":"2024 ","pages":"1386147"},"PeriodicalIF":2.0000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11461073/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Gastroenterology Research and Practice","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1155/2024/1386147","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Purpose: C-reactive protein (CRP) functions as a nonspecific marker in various inflammatory disorders, particularly in evaluating the efficacy of pharmacological treatments in patients with ulcerative colitis. The existing body of evidence does not offer adequate support for the direct implication of CRP in modulating the advancement of ulcerative colitis. Methods: Our study employed a rigorous mouse model. An ulcerative colitis mouse model was established by subjecting CRP-deficient 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. Results: 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-type 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-type mice. Conclusion: 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.
期刊介绍:
Gastroenterology Research and Practice is a peer-reviewed, Open Access journal which publishes original research articles, review articles and clinical studies based on all areas of gastroenterology, hepatology, pancreas and biliary, and related cancers. The journal welcomes submissions on the physiology, pathophysiology, etiology, diagnosis and therapy of gastrointestinal diseases. The aim of the journal is to provide cutting edge research related to the field of gastroenterology, as well as digestive diseases and disorders.
Topics of interest include:
Management of pancreatic diseases
Third space endoscopy
Endoscopic resection
Therapeutic endoscopy
Therapeutic endosonography.