[Impact of secondary lymphoid tissue chemokine on lymphocyte migration and the significance thereof in pathogenesis of ulcerative colitis: experiment with rats].
OBJECTIVE
To explore the impact of secondary lymphoid tissue chemokine (SLC) on lymphocyte migration and the significance thereof in the pathogenesis of ulcerative colitis (UC).


METHODS
Sixty SD rats were randomly divided into 3 equal groups: model group undergoing dripping of 40% acetone solution of dinitro-chlorobenzene (DNCB) on the back for 2 weeks and then enema of 6% DNCB acetone solution so as to establish models of UC, and then intravenous injection of normal saline (NS) for 5 days; SLC antibody intervention group undergoing intravenous injection of SLC antibody 15 microg x ml(-1) x kg(-1) immediately after the establishing of model; and control group undergoing enema of NS nly and then intravenous injection of NS for 5 days. Six days after the establishing of model venous blood samples were collected from the portal veins of the 3 groups. Lymphocytes were isolated and cultured. RT-PCR was used to detect the mRNA expression of the SLC receptor CCR7. Boyden chamber system was used to examine the migration ability of the lymphocytes exposed to SLC of 20, 40, 60, 80, and 100 ng/ml respectively. ELISA was used to detect the expression of interleukin (IL)-10 and interferon (IFN)-gamma in the supernatants of the lymphocytes of different groups.


RESULTS
RT-PCR showed that the CCR7 mRNA expression level of the model group was (0.792 +/- 0.108), significantly higher than that of the intervention group (0.386 +/- 0.115, P = 0.0429), and the CCR7 mRNA expression levels of these 2 groups were both significantly higher than that of the control group (0.106 +/- 0.029, both P < 0.01). SLC dose-dependently promoted the migration ability of the lymphocytes, but there existed a saturation phenomenon. Exposed to 80 ng/ml SLC the migration level of the lymphocytes of the model group peaked to (85.9 +/- 16.0), 3.7 times as high as that of the control group (20.5 +/- 1.8, P < 0.01), and the migration level of the lymphocytes of the intervention group was 38.2 +/- 6.3, significantly higher than that of the control group too (P < 0.05). SLC enhanced the expression of IFN-gamma of the lymphocytes of the model group, while reduced the IL-10 level, and both effects peaked at the concentration of 80 ng/ml (P = 0.042, P = 0.036).


CONCLUSIONS
SLC promotes the lymphocyte migration and boosts the differentiation of lymphocytes, thus participating in the pathogenesis of UC.
Ge
Bu-Jun
BJ
Department of Surgery, Tongji Hospital, Tongji University, Shanghai 200065, China. gebujun@126.com
Chen
Xi-Mei
XM
Yang
Chang-Qing
CQ
Wu
Jian
J
D000818:Animals; D002465:Cell Movement; D002478:Cells, Cultured; D054421:Chemokine CCL21 / Q000008:administration & dosage / Q000378:metabolism*; D003093:Colitis, Ulcerative / Q000276:immunology / Q000378:metabolism*; D005260:Female; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D008214:Lymphocytes / Q000166:cytology*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D054400:Receptors, CCR7 / Q000378:metabolism
C515372:Ccr7 protein, rat; D054421:Chemokine CCL21; D012333:RNA, Messenger; D054400:Receptors, CCR7; D016753:Interleukin-10; D007371:Interferon-gamma