Spondylarthropathy and gut inflammation: immunopathogenetic mechanisms

In 62% of patients with spondylarthropathy (SpA) we found clinically unsuspected gut inflammation to feature acute or chronic enterocolitis on ileocolonoscopy. A proportion of patients of the latter group had subclinical Crohn's disease as demonstrated clinically, endoscopically, genetically, histologically and immunopathologically. There is a relation between the activity of the gut inflammation and clinical rheumatic symptoms. A pathogenetic mechanism is increased handling of luminal (bacterial or nutritional) antigen, hence inducing T-cell activation and intestinal inflammation. In ileal mucosal biopsies we showed two different cellular events: increased enterocytic expression of class II molecules in active inflammation and an increase of membranous (M) cells overlying lymphocytes in inflamed mucosa. Although the number of intraepithelial lymphocytes was not increased in inflammation, intraepithelial T lymphocytes had protruding processes in close apposition to the tips of epithelial plasma membranes. Lymphocytes crossing the basement membrane were a frequent finding. These features indicate that the intestinal immune response caused by increased antigen processing in the terminal ileum induces an inflammatory immunocascade responsible for the clinical picture of SpA.