Studies on isolated gut mucosal lymphocytes in inflammatory bowel disease

Abstract

To determine whether a defective proliferation of gut mucosal lymphocytes is a contributory factor to the pathogenesis of inflammatory bowel disease, we assessed their reactivity toward mitogens and bacterial antigens. Spontaneous replication of intestinal lymphoid cells was higher than that of patient-matched peripheral blood lymphocytes. That gut mucosal lymphocytes appear to be activatedin loco was confirmed by a striking, time-dependent increase in the number of stable E rosettes generated by culturing unstimulated Crohn's disease intestinal lymphoid cells. The responses of lymphocytes from inflamed and normal mucosa to polyclonal mitogens were not only comparable to each other, but to those of corresponding peripheral lymphocytes, as well. Peripheral blood lymphocytes from patients with Crohn's disease showed less proliferation toBacteroides and lipopolysaccharide antigens than did those from control individuals, but replicated similarly in response toStaphylococcus aureus and the enterobacterial common antigen: In contrast, when cultured withStaphylococcus aureus or with lipopolysaccharides, gut mucosal lymphocytes from Crohn's disease proliferated 3–5 times more than did those from normal mucosa, while lymphoid cells from both sources were equally stimulated by the Kunin antigen. Overall, this study found no evidence for a defective proliferative capacity of immune competent cells at the gut mucosal level in inflammatory bowel disease.