Abstract
Inflammatory bowel disease (IBD) is a devastating relapsing-remitting systemic disease of the gastrointestinal system. It is characterized by an extremely imbalanced immune system and inflammatory mediators that result from the disruption of a complex series of interactions between the microbiome, the mucosal barrier, and the immune system. Over the past decades, numerous animal models such as chemical, genetic and bacterial models have populated to understanding pathophysiology of IBD and preclinical screening of therapeutic compounds for novel treatments. Among chemical-induced colitis models, the acetic-acid induced model is one of the legacy colitis models related to extensive hemorrhage, occasional ulceration, epithelium damage, and bowel wall thickening. Recently, Bahrami and his colleagues have reported the development of mucosal inflammation and intestinal fibrosis after exposure to 4% acetic acid for 10 min. Here, how their work addresses the importance of characterizing acetic-acid-induced colitis model to study the clinical features of IBD is commented.