Abstract

MODEL DEVELOPMENT OF DEXTRAN SODIUM SULPHATE INDUCED ULCERATIVE COLITIS IN FEMALE BALB/C MICE

Satyasri R. L.*, Sushma M. and Dr. V. Uma Maheswara Rao

ABSTRACT

Inflammatory bowel disease is the name of a group of disorders that cause the intestine to become inflamed. The inflammation last a long time and usually comes back over and over again. It is a complex multifactoial disease and commonly refers to ulceration colitis and crohn’s disease. Inflammatory bowel disease is common in developed countries with up to 1 to 200 of individuals in Northen Europian regions affected by these diseases. Colitis can occur from viral and bacterial infections, ischemic insult or autoimmune disorders; most notably Ulcerative colitis and crohn’s disease. Acute colitis may present with abdominal pain, distention, malabsortion, diarrhea, hematoschezia and mucus in the stool. We are beginning to understand the complex interactions between the environments, genetics factors. Inflammatory bowel disease and animal model of colitis have been essential in advancing our understanding of the disease. Although the causes, events initiating and triggering inflammation, and the precise immune regulatory defects of IBD are still not known, investigations have provided a better understanding of the mechanisms of perpetuation of inflammation, genetic susceptibility, tissue injury, and symptoms. Ulcerative colitis and Crohn's disease are related disorders that probably share susceptibility genes and have similar nonspecific inflammatory mediator profiles. These diseases, however, almost certainly have different causes and respond to different antigenic stimuli. It is probable that both ulcerative colitis and Crohn's disease represent heterogenic groups of diseases that share similar mechanisms of tissue damage but have different initiating events and immunoregulatory abnormalities. Rodent models demonstrate that a wide variety of initial injuries or perturbations of immunoregulatory pathways can lead to similar phenotypes of intestinal injury, and human studies show evidence of genetic heterogeneity. It is equally apparent from these models that initiating and perpetuating mechanisms are entirely distinct and that the intestine has a remarkable ability to heal.

Keywords: Crohn's disease, Ulcerative colitis, Hematoschezia, Inflammatory bowels disease, Dysplasia, Regional enteritis.