Purpose of review: Inflammatory bowel disease pathogenesis involves the interplay of multiple biological factors, among which nonimmune cells, including the endothelium, represent a crucial component of disease pathogenesis.
Recent findings: Endothelial cells play a key role in chronic inflammation through multiple and disparate activities. The mucosal microvasculature in inflammatory bowel disease is dysfunctional, overexpresses inflammatory molecules and undergoes intense angiogenesis, failing to exert its physiological antiinflammatory and anticoagulant activities.
Summary: The mucosal microcirculation is abnormal in inflammatory bowel disease and represents a novel component of disease pathogenesis; targeting the various abnormalities of the inflammatory bowel disease microcirculation may lead to new forms of therapeutic intervention.