{"title":"Filarial Parasite-Derived New Potential Bio-Therapeutic Agents For Inflammatory Bowel Diseases","authors":"V. Khatri, Nikhil Chauhan, R. Kalyanasundaram","doi":"10.31038/aghe.2019111","DOIUrl":null,"url":null,"abstract":"Inflammatory Bowel Disease (IBD) comprising of Crohn’s disease (CD) and Ulcerative Colitis (UC), is a chronic and relapsing inflammatory condition of the gastrointestinal tract [1]. There has been an alarming increase in the incidence of IBD during the past decade, leading to long-term morbidity that considerably affects the quality of patient’s life [1]. The incidence of UC has been rising globally since the mid-20th century [2]. Genetic factors are thought to play an important role in the pathogenesis of UC. Studies by Bengtson et al. [3] showed that the risk of developing colitis rises by 4.6-fold when a sibling has colitis. Similarly, if one of the monozygotic twins develops colitis, the risk of the other twin developing the disease is relatively 95 times higher [4]. Dietary factors have also been reported to play a role in the development of colitis. A diet containing high amounts of refined fat, meat, and sugar are risk factors for developing colitis [5]. Unfortunately, the mainstream therapies available currently for treating colitis are largely non-specific with short-term immunosuppressive effect and nearly all of them predispose the patients to opportunistic infections and/or increased risk for cancer development [6]. The most preferred method for treating mild to moderate UC is the administration of 5-aminosalicylates (5-ASA). Patients suffering from moderate to severe UC or those who do not respond to 5-ASA can be treated with antibiotics or corticosteroids but these treatment options come with various side effects like nausea, headache, diarrhea, insomnia, osteoporosis, and non-Hodgkin lymphoma [7, 8]. Similarly, anti-TNF-α therapy against UC is associated with the risk of hepatosplenic T cell lymphoma [9] and the effect of anti-TNF-α therapy reduces with time [10]. Recent advances to study the mechanism of inflammation in UC has provided a better understanding of the underlying molecular basis of the disease, which is helping in the development of new therapeutic approaches for UC [11, 12].","PeriodicalId":276878,"journal":{"name":"Advancements in Gastroenterology, Hepatology and Endoscopy","volume":"165 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advancements in Gastroenterology, Hepatology and Endoscopy","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.31038/aghe.2019111","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Inflammatory Bowel Disease (IBD) comprising of Crohn’s disease (CD) and Ulcerative Colitis (UC), is a chronic and relapsing inflammatory condition of the gastrointestinal tract [1]. There has been an alarming increase in the incidence of IBD during the past decade, leading to long-term morbidity that considerably affects the quality of patient’s life [1]. The incidence of UC has been rising globally since the mid-20th century [2]. Genetic factors are thought to play an important role in the pathogenesis of UC. Studies by Bengtson et al. [3] showed that the risk of developing colitis rises by 4.6-fold when a sibling has colitis. Similarly, if one of the monozygotic twins develops colitis, the risk of the other twin developing the disease is relatively 95 times higher [4]. Dietary factors have also been reported to play a role in the development of colitis. A diet containing high amounts of refined fat, meat, and sugar are risk factors for developing colitis [5]. Unfortunately, the mainstream therapies available currently for treating colitis are largely non-specific with short-term immunosuppressive effect and nearly all of them predispose the patients to opportunistic infections and/or increased risk for cancer development [6]. The most preferred method for treating mild to moderate UC is the administration of 5-aminosalicylates (5-ASA). Patients suffering from moderate to severe UC or those who do not respond to 5-ASA can be treated with antibiotics or corticosteroids but these treatment options come with various side effects like nausea, headache, diarrhea, insomnia, osteoporosis, and non-Hodgkin lymphoma [7, 8]. Similarly, anti-TNF-α therapy against UC is associated with the risk of hepatosplenic T cell lymphoma [9] and the effect of anti-TNF-α therapy reduces with time [10]. Recent advances to study the mechanism of inflammation in UC has provided a better understanding of the underlying molecular basis of the disease, which is helping in the development of new therapeutic approaches for UC [11, 12].