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Studies on isolated gut mucosal lymphocytes in inflammatory bowel disease. Detection of activated T cells and enhanced proliferation to Staphylococcus aureus and lipopolysaccharides.
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 activated in 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 to Bacteroides and lipopolysaccharide antigens than did those from control individuals, but replicated similarly in response to Staphylococcus aureus and the enterobacterial common antigen: In contrast, when cultured with Staphylococcus aureus or with lipopolysaccharides, but 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 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.
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