Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis typically begins as a response to a combination of immunological, genetic, or environmental factors.

These factors lead to disruption of the protective mucus layer that normally lines the colon.

This is accompanied by dysfunction of epithelial tight junctions, resulting in increased intestinal permeability.

In response to this breach, the immune system is activated. Various immune cells, including neutrophils, lymphocytes, plasma cells, macrophages, and eosinophils, are recruited to the colonic mucosa.

These cells release pro-inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1, interleukin-6, and interleukin-13.

As the inflammatory process progresses, neutrophils infiltrate the crypts of Lieberkühn—tubular glands in the colon, leading to the formation of crypt abscesses and the destruction of glandular tissue.

This damage reduces the colon’s ability to absorb water and electrolytes, contributing to diarrhea. Concurrently, mucosal ulceration and capillary fragility lead to rectal bleeding.