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Interleukin-33 orchestrates an immune network to counteract severe acute colitis
Inflammatory bowel disease (IBD) is mainly characterized by mucosal damage and ulceration, which are both considered to be high-risk conditions for the development of colorectal cancer. Globally, around 6.8 million people are suffering from IBD, with increasing prevalence. Despite extensive research investigating the pathogenesis of IBD, the precise etiology is still unknown and no curative therapy has been developed so far. Due to this fact, current therapies mainly focus on alleviating and suppressing clinical manifestations like recurring diarrhea, excessive abdominal pain and pronounced body weight loss. Even though drugs for the treatment of IBD have reached remarkable progress, only less than half of the patients show an efficient response. To improve the patients’ quality of life and to avoid unwanted complications like surgery or even the development of bowel cancer, it is of essential importance to develop new therapeutic approaches. Recently, interleukin-33 (IL-33) and its receptor ST2 have emerged as important modulators in inflammatory disorders. Especially in the context of intestinal inflammation, several studies have emphasized the IL-33/ST2 signaling pathway as a key target for therapeutic strategies. Nevertheless, findings obtained so far did not achieve conclusive results about the IL-33 function in the intestine. Therefore, we investigated the role of IL-33 during intestinal inflammation and further elucidated its potential as a novel therapeutic drug. Interestingly, the expression of IL-33, but not its receptor ST2, was significantly enhanced in inflamed intestinal lesions of IBD patients compared to non-inflamed tissues. Well in line, mice with Dextran Sulfate Sodium (DSS)-induced colitis exhibited a strong increase of IL-33 expression in the colon compared to healthy control mice. Mice deficient for ST2 displayed an aggravated colon pathology compared to wild type mice, suggesting a favorable function of IL-33 during colitis. Indeed, exogenous IL-33 treatment resulted in a tremendous ...
Interleukin-33 orchestrates an immune network to counteract severe acute colitis
Inflammatory bowel disease (IBD) is mainly characterized by mucosal damage and ulceration, which are both considered to be high-risk conditions for the development of colorectal cancer. Globally, around 6.8 million people are suffering from IBD, with increasing prevalence. Despite extensive research investigating the pathogenesis of IBD, the precise etiology is still unknown and no curative therapy has been developed so far. Due to this fact, current therapies mainly focus on alleviating and suppressing clinical manifestations like recurring diarrhea, excessive abdominal pain and pronounced body weight loss. Even though drugs for the treatment of IBD have reached remarkable progress, only less than half of the patients show an efficient response. To improve the patients’ quality of life and to avoid unwanted complications like surgery or even the development of bowel cancer, it is of essential importance to develop new therapeutic approaches. Recently, interleukin-33 (IL-33) and its receptor ST2 have emerged as important modulators in inflammatory disorders. Especially in the context of intestinal inflammation, several studies have emphasized the IL-33/ST2 signaling pathway as a key target for therapeutic strategies. Nevertheless, findings obtained so far did not achieve conclusive results about the IL-33 function in the intestine. Therefore, we investigated the role of IL-33 during intestinal inflammation and further elucidated its potential as a novel therapeutic drug. Interestingly, the expression of IL-33, but not its receptor ST2, was significantly enhanced in inflamed intestinal lesions of IBD patients compared to non-inflamed tissues. Well in line, mice with Dextran Sulfate Sodium (DSS)-induced colitis exhibited a strong increase of IL-33 expression in the colon compared to healthy control mice. Mice deficient for ST2 displayed an aggravated colon pathology compared to wild type mice, suggesting a favorable function of IL-33 during colitis. Indeed, exogenous IL-33 treatment resulted in a tremendous ...
Interleukin-33 orchestrates an immune network to counteract severe acute colitis
Ngo Thi Phuong, Nhi (Autor:in) / Westendorf, Astrid
21.07.2021
Hochschulschrift
Elektronische Ressource
Englisch
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