Objective To investigate the role of Th17 cells and related cytokines in Helicobacter pylori(H.pylori) infection.Methods To establish a mouse model of H.pyloriinfectious gastritis.Meanwhile,a treatment group and control group were set up.The histological changes in the gastric mucosa were observed and scored under light microscopy;The expression of IL-17 and IL-23 mRNAs as well as protein in gastric tissue was detected by RT-PCR and ELISA,respectively;Th17 cells in mice splenocyte were evaluated using the flow cytometry (FCM) method.Results We found significantly higher levels of IL-17 and IL-23 protein and mRNA levels in supernatant of gastric tissue homogenates of infection group as compared to controls and Th17 cells in spleen from mice of H.pylori infection group were all obviously higher than that of control group;IL-17 mRNA,IL-23 mRNA and the ratio of Th17 cells in mice splenocyte of H.pylori infection group mice increased gradually with the time prolonged;The levels of both mRNA and protein levels of IL-17and IL-23 decreased significantly in the treatment group compared with pre-treatment;There was a positive correlation between IL-17 and IL-23 expression levels of mice gastric mucosa and gastric inflammation degree.Conclusion H.pylori infection induced the immune response of Th17 cells;The levels of IL-17 and IL-23 increased in gastric mucosa of mice after H.pyloriinfection;The degree of H.pylori-infected mice gastric inflammation was positive correlation with the levels of IL-17 and IL-23 of gastric mucosa.

To predict and identify the dominant B‐cell epitopes of conserved region of Treponema pallidum repeat protein F (TprFN ) and provide the basis for development of polyvalent epitope‐based syphilis vaccine ,the amino acid sequence of TprFN was obtained from GenBank and analyzed with comprehensive meta‐analysis Mobyle ,ABCpred and IEDB online software .The peptides containing predicted epitopes were artificially synthesized . To obtain and measure the titers of antibodies against TprFN ,New Zealand rabbits were immunized with recombinant protein TprFN expressed in E .coli and identified by Western blot (WB) .Sera from TprFN‐immunized rabbits ,syphilis patients ,and normal human and normal rabbits were used to deter‐mine the immunoreactivity and specificity of 7 predicted peptides of TpFN by indirect ELISA .Comprehensive meta‐analysis of online software showed that P1 (43‐62AA) ,P2(57‐71AA) ,P3(81‐88AA) ,P4(89‐103AA) ,P5(125‐138AA) ,P6(231‐251AA) and P7(268‐279AA) might be the B‐cell epitopes .A protein was expressed in a soluble form and identified as TpFN by WB .The ELISA indicated that P1 and P3 were active with TprFN‐immunized rabbit sera and syphilis patient sera but not with negative control sera .These results indicate that P1 and P3 are the potential dominant B‐cell epitopes .

Abstract] Objective To study the roles of IL-12 and IL-23 in the development of protective im-munity and pathological changes during chlamydial urogenital infection.Methods C57BL/6J wild type (wt) mice and mice deficient in IL-12p35 (IL-12p35 KO) or IL-12p40 (IL-12p40 KO)were inoculated in-travaginally with 1×104 IFU of live Chlamydia muridarum ( C.muridarum) organisms.Half mice of each group were reinfected on day 114 after primary infection.Vaginal swabs were taken every 3 or 4 days to mo-nitor live organism shedding.The mice were sacrificed after 114 or 143 days of primary infection and the va-ginal tract and kidney samples were collected for pathological analysis.The numbers of chlamydial inclusion bodies and bacteria in kidney homogenates were titrated after 100 days of primary infection.Results The infection time courses of mice deficient in either IL-12p35 or IL-12p40 were similar after primary infection, but were prolonged as compared with the wild type mice.All mice regardless of genotypes developed severe pathological damages in upper genital tracts with no significant difference among different groups.Almost all IL-12p40 KO mice and some IL-12p35 KO mice showed pathological changes in kidney samples.No obvious abnormality was observed in any of the kidneys from wild type mice.Neither the age-matched IL-12p35 KO nor IL-12p40 KO mice developed any gross pathological changes in kidney in the absence of chlamydial in-fection.C.muridarum inclusions were detected in kidney samples with gross pathological damages from IL-12p35 KO mice and IL-12p40 KO mice.No inclusions were ever detected in kidneys from the wild type mice.The numbers of chlamydial inclusions in the IL-12p40 KO mice were much higher than those of the IL-12p35 KO mice.Live bacteria were detected in mice deficient in either IL-12p35 or IL-12p40, but not in the wild type mice.No significant difference with the number of live bacteria was found between IL-12p35 KO mice and IL-12p40 KO mice.Conclusion IL-12 and IL-23 could inhibit the spread of C.muridarum in-fection from genital tract to kidney.The deficiency of IL-12 or IL-23 might relate to the renal lesions induced by Chlamydia infection.