Effect of Mycobacterium phlei F.U.36 on balance of CD4+CD25+ regulatory T cells and Th17 cells in asthmatic mice

Abstract:

OBJECTIVE: To evaluate the effect of early intervention with Mycobacterium phlei F.U.36 injection on the balance of CD4+CD25+ regulatory T cells and Th17 cells in asthmatic mice, and to investigate the immunomodulatory effect of Mycobacterium phlei F.U.36. METHODS: Thirty female BALB/c mice were randomly divided into three groups: normal control (n=10), asthma model (n=10) and Mycobacterium phlei F.U.36 treatment groups (n=10). A mouse model of asthma was prepared by injection and aerosol inhalation of chicken ovalbumin in the asthma model and Mycobacterium phlei F.U.36 treatment groups, while mice in the normal control group were given normal saline instead. The treatment group was intraperitoneally injected with Mycobacterium phlei F.U.36 (0.57 μg, once every other day) three times in the first two weeks after the first sensitization. All mice were sacrificed at 24 hours after the last challenge. Left lung tissues of these mice were obtained and made into sections for observation of inflammatory changes. The percentages of CD4⁺CD25⁺ regulatory T cells and Th17 cells in CD4⁺ T cells among splenic mononuclear cells were determined by flow cytometry. The levels of interleukin (IL)-10 and IL-17 in serum and bronchoalveolar lavage fluid were measured using ELISA. Results Compared with the normal control group, the asthma model group had significantly decreased percentages of CD4⁺CD25⁺ regulatory T cells and IL-10 levels (P<0.05) and significantly increased percentages of Th17 cells and IL-17 levels (P<0.05). Compared with the asthma model group, the Mycobacterium phlei F.U.36 treatment group had significantly increased percentages of CD4⁺CD25⁺ regulatory T cells and IL-10 levels (P<0.05) and significantly decreased percentage of Th17 cells and IL-17 levels (P<0.05). Conclusions Early intervention with Mycobacterium phlei F.U.36 can promote development of CD4⁺CD25⁺ regulatory T cells and production of IL-10 and inhibit generation of Th17 cells and production of IL-17 in asthmatic mice.