The Study Of Systemic Inflammation And Inflammatory Pathways Of DSS Induced Models Of Mice Colitis

Objective:10 DSS induced acute and chronic models of mice colitis and 10 negative controls as materials, we detected DAI, gut barrier function and inflammatory indicators to assess intestinal permeability change and intestinal mucous membrane impairment level, and we detected colon length, spleen weight and different levels of plasma inflam-matory proteins by protein microarray to explore the approach of enterogenic infection.Methods: thirty 17 weeks old nude mice were randomized to three groups, including acute, chronic and control group, each group of 10. During the experiment, we weighed mice, assessed stool character and test faecal occult blood everyday. After experiment, we killed mice and got colon length and spleen weight. We assess colon mucosa histo-pathological changes by HE coloration, serum DAO level by ultraviolet spectrophotom-etry, DLAC by colorimetry and different plasma inflammatory proteins by protein mi-croarray, including BLC, CD30L, Eotaxin, Eotaxin-2, Fas Ligand, Fractalkine, GCSF, GM-CSF, IFNγ, IL-1α, IL-1β, IL-2, IL-3, IL-4, IL-6, IL-9, IL-10, IL-12p40p70, IL-12p70, IL-13, IL-17,I-TAC, KC, leptin, LIX, lymphotactin, MCP-1, MCSF, MIG, MIP-1α, MIP-1γ, RANTES, SDF-1, TCA-3, TECK, TIMP-1, TIMP-2, TNFα, sTNFRI, sTNFRII.Results: comparing with negative control group, the acute (P=0.0013) and chronic group (p=0.0000) had significantly lower body index, and there was no significance for body index between acute and chronic groups (P=0.8720); the acute (P=0.0114) and chronic group (P=0.0001) had significantly higher DAI than control group, and there was no significance between acute and chronic groups (P=0.5061); comparing with neg-ative control group, there was no significance for DAO either acute (p=0.6125) or chronic group (p=0.2898); acute group had not significantly higher serum DLAC level than control group (P=0.1221), chronic group had significantly higher serum DLAC level than control group (P=0,0412), chronic group had not significantly higher serum DLAC level than acute group (P=0.3198); acute (P=0.0002) and chronic group (P=0.0001) had significantly higher colon mucosa histopathological score than control group, and there was no significance between acute and chronic groups (P=0.4711); acute (P=0.0004) and chronic group (p=0.0002) had significantly shorter colon length than control group, and there was no significance between acute and chronic groups (p=0.0765); comparing with negative control group, there was no significance for spleen weight index (spleen weight/body weight) either acute (P=0.3087) or chronic group (P= 0.8605); acute group had significantly higher level of sTNFRII (P=0.0425), KC (P=0.0372), MIG (P=0.0340) and not significantly higher level of sTNFRI (P=0.0511), TIMP-2 (P=0.0721) than control group, chronic group had significantly higher level of sTNFRII (P=0.0433) and not significantly higher level of sTNFRI (P=0.1734), KC (P=0.7715), MIG (p=0.0833) than control group, and acute group had significantly higher level of TIMP-2 than chronic group (P=0.0228).Conclusions:We successfully constructed DSS induced acute and chronic models of mice colitis, and screened 4 inflammatory proteins which were involved in inflamma-tory pathways in enterogenic infection by protein microarray, including sTNFRII, KC, MIG and TIMP-2. Our study preliminarily clarified the role of each inflammatory pro-tein in enterogenic infection and their machanisms, laying foundation for the further re-search.