Immune regulation of IL-10 to Schistosoma japonicum infection in p47 GTPase deficient mouse model / 中国血吸虫病防治杂志

ABSTRACT

Objective To investigate the immune response of IL-10 to Schistosoma japonicum infection in the early infectioin model and SEA immunization model of the IGTP~(-/-) and IRG-47~(-/-) mice.Methods In the early infection model,the IGTP knock out (IGTP~(-/-)) mice,IRG-47 knock out (IRG-47~(-/-)) mice and wild-type (WT) C57BL/6J mice were exposed to 300 S.japonicum cercariae via the pinna and sacrificed on day 7 post-infection.Each mouse pinna section was stained with hematoxylin-eosin (HE) to detect the pathological lesions,and the culture supernatant of pinna was used to test the levels of Th1/Th2 cytokines by indirect ELISA.In the SEA immunization model,IGTP~(-/-) IRG-47~(-/-) and WT mice were immunized with SEA twice and sacrificed in 3 weeks after the initial immunization.SEA-specific IgG antibody in sera was detected by indirect ELISA;the levels of Th1/Th2 cytokines were tested in culture supernatant of splenocytes by indirect ELISA;the proportions of CD4~+ T cells,CD8~+ T cells,B cells,Th1 and Th2 cells in the spleen were assayed by FACS.Results Although no obvious differences on the pathology of pinna were observed among the three mouse groups,the level of IL-10 in the culture supernatant of pinna of IRG-47~(-/-) mice was lower than that of IGTP~(-/-) mice in 7 days after the exposure.Following SEA immunization,the level of SEA-specific IgG antibody in sera of IGTP~(-/-) mice was lower than that in WT mice,the level of IL-10 in the culture supernatant of splenocytes of IRG-47~(-/-) mice was higher than that of IGTP~(-/-) and WT mice with the stimulation of SEA.However,the proportion of Th2 cells in the spleen of IRG47~(-/-) mice was the lowest among the three mouse groups.Conclusions SEA is the stimulus of IRG-47 deficiency mice to defend Schistosoma japanicum infection and promote the host to produce a protective response,and IL-10 may play an important role in immune regulation in this process.