[Abnormal lymphocyte homing and colon lesions in ulcerative colitis: experiment with rats].

OBJECTIVE: To investigate the relationship between abnormal lymphocyte homing and colon lesions in ulcerative colitis. METHODS: 60 Sprague-Dawley rats were randomly divided into 3 equal groups: model group [undergoing enema of dinitrochlorobenzene to establish models of ulcerative colitis and then venous injection of normal saline (NS) once a day for 5 days], lymphocyte homing intervention group [undergoing venous injection of secondary lymphoid-tissue chemokine (SLC) antibody, and then venous injection of NS for 5 days], and control group [undergoing venous injection of NS for 5 days]. On the 6th day blood samples were collected from the portal vein to isolated lymphocytes. Distant colon was dissected to undergo pathological examination of submucosal aggregated lymphatic follicles, ulceration, and inflammation, thus observing the lymphocyte homing situation. Specimens of colon mucosa underwent detection cytokine of interleukin (IL)-2 and IL-6. RT-PCR was used to detect the mRNA expression of SLC gene and the chemokine receptor CCR7. The proportion of CCR7 positive lymphocytes which drainage from colonic vein were measured by flow cytometry (FC). RESULTS: Abnormal lymphocyte homing phenomenon under colonic mucosa was found in the model and intervention groups. The relative grey degree of SLC gene mRNA expression of the model and intervention groups were 0.85 +/- 0.05 and 0.77 +/- 0.14 respectively, both significantly higher than that of the control group (0.31 +/- 0.11, both P < 0.01), however, without significant difference between the 2 former groups. The relative grey degree of CCR7 mRNA expression of the model group was 0.79 +/- 0.11, significantly higher than that of the intervention groups (0.39 +/- 0.12, P = 0.0429), and both were significantly higher than that of the control group (0.11 +/- 0.03, both P < 0.01). FC showed that the proportion of CCR7(+) lymphocytes drainage from colonic vein of the model and the intervention groups were 69% +/- 5% and 77% +/- 10% respectively, both significantly higher than that of the control group (17% +/- 84%, both P < 0.01), however, without significant difference between these 2 former groups (P = 0.0837). CONCLUSION: Abnormal lymphocyte homing is associated with inflammation of the colonic mucosa. Blocking of the lymphocyte homing is effective in reducing the inflammation of colonic mucosa.