Background: Rheumatoid Arthritis (RA) is a common chronic autoimmune diseasewith high morbidity and disability, the current treatment is mainly symptomatictreatment to reduce the level of pain the patient and slowing disease progression, butstill no effective cure program. Currently believed that RA is due to Th1/Th2and ofTh17/Treg immune imbalance caused by autoimmune disorders, correct the immuneimbalance can treat or prevent RA. In recent years, the study found that: the trichinellaspiralis infection strong advantage of Th2immune response can stimulate the host, Th1/Th2balance caused by axial Th2deviation, thus reducing part Th1mediated theoccurrence and development of autoimmune diseases and pathological damage.But hasyet to see the action of the RA or research reports, we hypothesized that trichinellaspiralis infection may also through the immune adjustment also play a role for RA.Objective:(1) In this study, attempts to observe Trichinella spiralis infection CIAmouse model of disease, the impact of the development process.(2) To investigate thetrichinella spiralis infection on immune regulation mechanism of the CIA model inmice.Methods:(1) By CII emulsified with Freund’s adjuvant emulsion to induce arthritisDBA-1mice, build collagen-induced arthritis in mice (CIA) model, keeping theenvironment under the SPF level. Trichinella spiralis muscle larvae (300/mouse) wereadministered orally infected mice.(2) Arthritis incidence of mice was observed, and theclinical observation index observation, grading, judge the trichinella spiralis infectionaffected the CIA mice at different group.(3) The shearing DBA-1foot claws and kneejoint parts for pathological section, HE staining to observe the pathological damagedegree of difference between different groups.(4) ELISA method to detect the miceserum CII IgG1, IgG2a collagen and its sub-types specific IgG antibody levels.(5)3H-TdR incorporation method detecting spleen lymphocyte proliferation response.(6) flow cytometry test mice spleen lymphocytes Th1, Th2, Th17, Treg cells.and Foxp3.Results:(1)Compared with the control group of normal mice CIA model micesignificantly inflamed paw parts and mice activity.(2) Compared with the model groupCIA, CIA group advance Trichinella infection, a: CIA mice can significantly reducearthritis disease, reduce the pathological damage. b: CⅡcollagen-specific serum IgG,IgG2a levels were significantly reduced, increased IgG1levels. c: polyclonal ConAstimulated spleen lymphocytes and antigen-specific stimulation of CⅡ-inducedproliferative response was significantly reduced. CIA group also infected withTrichinella spiralis and morbidity of the disease, as well as CⅡcollagen serum IgG andits subclasses not significantly affected. Trichinella infection CIA group delay increasedarthritis severity and pathological damage.(3) Compared with the CIA model controlgroup, the CIA building before2weeks trichinella spiralis infection group of Th1andTh17cells ratio decreased significantly, the Th2and Treg cells rates also increasedsignificantly.The CIA made mould and trichinella spiralis infection group and the CIAmodel after2weeks Th1, Th2of trichinella spiralis infection group, the percentage ofTh17and Treg cells subgroup the CIA model control group no significant difference.Conclusions:(1) Pre-trichinella infection can reduce the clinical symptoms of theCIA and reduce pathological damage, damage to the articular pathology play aprotective role.(2) Trichinella spiralis of CIA mice model of protection depends on thetrichinella spiralis infection in advance by starting Th2, Treg response to suppress theheterogeneous type Ⅱ collagen induced pathogenic Th1and Th17response. |