Migration inhibitory factor is involved in experimental colitis induced by intrathecal injection of haptten to rat.
- Author:
Xing-Yu WU
1
;
Hui PAN
;
Lin MEI
Author Information
1. Department of Physiology and Pathophysiology, Peking University Health Science Center, Beijing, 100083, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Antibodies;
pharmacology;
Colitis, Ulcerative;
chemically induced;
metabolism;
Haptens;
adverse effects;
Injections, Spinal;
Macrophage Migration-Inhibitory Factors;
metabolism;
Rats
- From:
Acta Physiologica Sinica
2008;60(3):419-424
- CountryChina
- Language:Chinese
-
Abstract:
In recent years, there has emerged academic tendency towards the neurogenic mechanism of ulcerative colitis (UC). As one of the supports to the hypothesis of UC being a neurogenic inflammation, we have built a colitis model by intrathecal (ith) injection of a haptten 2,4-dinitrochlorobenzene (DNCB) to DNCB-sensitized rats. In order to explore further the neuroimmunal mechanism of this colitis model, we here focused on a pro-inflammatory cytokine, migration inhibitory factor (MIF), to observe its expression in rat colon nervous tissue and spinal cord in the colitis induced by ith injection of DNCB. At the same time we also observed the effect of MIF antibody pretreatment on the disease active index (DAI) score and the colon pathology by HE staining in the colitis rats. The results obtained showed that the immunofluorescence intensity of double staining of MIF protein in colon nervous tissue and spinal cord was increased in 0.8% and 1.6% DNCB-induced colitis groups than that in the control (60% ethanol) group. Both the colon pathology and the DAI score were significantly reduced by MIF antibody ith pretreatment. Ith injection of 0.8% DNCB after MIF antibody (1:10, 1:5) pretreatment could only induce lower DAI score (P<0.01 as compared, respectively, to the IgG pretreatment group). The colon pathological changes in ith 0.8% DNCB rats were mild, even little after MIF antibody (1:10, 1:5) pretreatment. These results suggest that MIF in spinal cord and enteric nervous system is possibly involved in the rat colitis induced by ith injection of DNCB, which reflects a neuroimmunal mechanism underlying this kind of colitis. MIF is possibly one of the important neurochemical factors in this experimental colitis, even in the UC.
