Effects Of Schistosome Japonicum Polygyrus On CD4+T Cell In CD4⁺CD45RB^hiT Cell-mediatedenterifis Mice Model

ObjectiveObservation the effect of Schistosoma japonicum on murine enteritis in CD4+Tcell secretion and infiltration, and preliminary study of Schistosoma japonicum in thetreatment of inflammatory bowel disease in mouse.MethodsUse of flow cytometric screening of CD4⁺CD45RB^hi T cells into SCID MiceColitis in mice model of production. The experimental mouse model for Schistosomajaponicum infection group and experimental colitis group, observe two groups ofmice’s body weight, color, motion and changes in stool, colonic inflammationhistological pathology; with immunofluorescence method to observe infection in2weeks,4weeks,6weeks in the CD4+T mouse colon tissue infiltration; application ofreal-time fluorescence quantitative PCR detection of infection in2weeks,4weeks,6weeks in colon tissue of mouse interferon gamma （IFN-γ） and interleukin-4（IL-4）mRNA expression.Results1.general situation: different time points in two groups of mice showed varyingdegrees of weight loss, diarrhoea, lazy, arch, anorexia. The two groups of mice haircolor were significantly dimmed, fecal pulpy,6weeks of infection group appeared in 1cases prolapse of the anus.2.Immunofluorescence: In the infected group, mouse early metaphase T cellsincreased significantly, but with the extension of infection, the T cell expression wassignificantly decreased. In inflammatory group, mice of T cells expressing intosustained growth. While the infection group and the inflammatory group comparisonat2weeks and4weeks group, groups of mice infected with colonic tissue CD4+Tcells expressing a inflammation group increased （P <0.05）; but6weeks groupinfection group CD4+T cells expressing a inflammatory group decreased significantly（P <0.01）.3.RT-PCR: The infected group of colonic tissue in IL-4mRNA expressed duringthe infection process continued to increase, at4weeks,2weeks group wassignificantly greater than the expression （RQ=5.15±0.36, RQ>2, P <0.01）, at6weeks,2weeks group with the same expression was increased （RQ=12.12±0.65, RQ>2, P <0.01）,6weeks and4weeks compared with similarly elevated （RQ=2.29±0.74, RQ>2, P <0.01）. Infection with group IFN-γ mRNA expression in4weeks is2weeks increased expression （RQ=3.73±0.17, RQ>2, P <0.01）, but in6weeks when expression is2weeks reduced （RQ=0.47±0.28, RQ <0.5, P <0.01）,while a4weeks of expression also decreased significantly （RQ=0.12±0.53, RQ <0.5,P <0.01）. In inflammatory group, IL-4mRNA expression in2and4weeks （RQ=0.36±0.24, RQ <0.5）,6weeks （RQ=0.362±0.43, RQ <0.5, P <0.05） compared aredecreased, but in the mid to late expression but no obvious abnormality of RQ=1.004±0.49,0.5<RQ <2, P>0.05); while the IFN-γ expression of mRNA wereincreased （RQ=2.67±0.16, RQ>2, P <0.05; RQ=8.46±0.72, RQ>2, P <0.05, RQ=3.16±0.74, RQ>2, P <0.05）. In two experiments comparing group in2weeks, theinfection group IL-4mRNA expression was significantly reduced the inflammatorygroup （RQ=0.45±0.99, RQ>2, P <0.05）, but IFN-γ mRNA expression wassignificantly increased （RQ=2.51±0.49,0.5<RQ <2, P <0.05）, at4weeks, theinfection group IL-4mRNA expression was significantly elevated,（RQ=9.31±0.43,RQ>2, P <0.05）, and IFN-γ mRNA expression increased gamma （2.62±0.23, RQ>2,P <0.05）, at6weeks, infection and inflammation group than in the group IL4therelative number of （RQ=22.78±0.78, RQ>2, P <0.05）, but IFN-γ mRNAexpression was significantly lower （RQ=0.03±0.88, RQ <0.5, P <0.05）. ConclusionSchistosoma japonicum infection early、metaphase, May to class Th1immuneresponse mainly, strengthen the IFN-γ expression, resulting in Th2/Th1imbalance,which causes CD4+T cell secretion and infiltration of the aggravate, caused by theincrease of murine intestinal inflammation. Schistosoma japonicum infection to later,immune responses to Th2mainly, in promoting IL-4expression at the same timethrough a gradual inhibition of IFN-γ expression, strengthening the induction ofTh2and inhibition of Th1, Th1/Th2balance, ease of murine intestinal inflammation.