JOURNAL ARTICLE

[Relationship between CD4 + CD25 + Foxp3 + regulatory T cells and Th17 responses in Chlamydia muridarum pulmonary infection]

Xiaojing Zhou, Lixiang Chen, Wangzhan Zhou, Jun Huang, Danhui Liu, Wenjiang Zhou, Yunwen Hu, Jianxin Lv, Xiaohui Zhou
Wei Sheng Wu Xue Bao, Acta Microbiologica Sinica 2013 January 4, 53 (1): 74-81
23614243

OBJECTIVE: To study the relationship between CD4 + CD25 + Foxp3 + regulatory T cells and Th17 responses during pulmonary infection of Chlamydia muridarum (Cm) in BALB/c mice. [Methods] BALB/c mice aged 6-8 weeks were inoculated intranasally with 5 x 103 IFU of Cm to set up the murine model of Chlamydial pneumonia. The boet weight changes, the growth of Cm and the pathology in the lung were monitored at different time post-infection. In determine the CD4 + CD25 + Foxp3 + regulatory T cells responses in BALB/c mice, intracellular cytokine staining was used to assay the percentage of CD4 + CD25 + Foxp3 + T cells in the spleen and mediastinum lymph node (MLN). The production of cytokines/chemokines in the lung were monitored, including IL-6,TGF-beta,IL-17 ,IL-2 (by ELISA), K(C and MIP-2 (by RT-PCR).

RESULTS: Intranasally infected with 5 x 10(3) IFU of Cm in mice resulted in chlamydial pneumonitis featured by body weight lost, chlamydia growth and pathological damage in the lung compared with their uninfected counterparts. On day 3 post-infection, the percentage of CD4 + CD25 + Foxp3 + T cells in the spleen and MLN were significantly decreased than the control mice; then began to increase and recover to the original level on day 7 post-infection. The production of Th17 associated cytokines/chemokines such as IL-6, IL-17, KCand MIP-2 increased, which peaked on day 7 post-infection, then gradually reduced. The production of TGF-beta and IL-2 was consistent with the trend of CD4 + CD25 + Foxp3 + T cells.

CONCLUSION: During pulmonary infection of Cm in BALB/c mice, CD4 + CD25 + Foxp3 + regulatory T cells may promote type 17 T cell immunity through providing TGF-beta in the presence of IL-6.

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