
Radical induction theory of ulcerative colitis
Author(s) -
Jay Pravda
Publication year - 2005
Publication title -
world journal of gastroenterology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v11.i16.2371
Subject(s) - ulcerative colitis , pathogenesis , immunology , immune system , inflammatory bowel disease , colitis , inflammation , intestinal mucosa , submucosa , lamina propria , extracellular , chemistry , pathology , microbiology and biotechnology , medicine , biology , epithelium , disease , biochemistry
To propose a new pathogenesis called Radical Induction to explain the genesis and progression of ulcerative colitis (UC). UC is an inflammatory bowel disease. Colonic inflammation in UC is mediated by a buildup of white blood cells (WBCs) within the colonic mucosal lining; however, to date there is no answer for why WBCs initially enter the colonic mucosa to begin with. A new pathogenesis termed "Radical Induction Theory" is proposed to explain this and states that excess un-neutralized hydrogen peroxide, produced within colonic epithelial cells as a result of aberrant cellular metabolism, diffuses through cell membranes to the extracellular space where it is converted to the highly damaging hydroxyl radical resulting in oxidative damage to structures comprising the colonic epithelial barrier. Once damaged, the barrier is unable to exclude highly immunogenic fecal bacterial antigens from invading the normally sterile submucosa. This antigenic exposure provokes an initial immune response of WBC infiltration into the colonic mucosa. Once present in the mucosa, WBCs are stimulated to secrete toxins by direct exposure to fecal bacteria leading to mucosal ulceration and bloody diarrhea characteristic of this disease.