Since all three of these strains (especially strain 288) caused degradations of ZO-1, ZO-2, ZO-3, and claudin-7 after infection with the T84 monolayer, we suspect that ASP produced outside the cells may cause or contribute to (i) the degradation of these protein components and (ii) a decrease in the barrier function of the T84 intestinal epithelial cells. The gene discussed is TJP1; the disease is infection.