[Expression of interleukin-21 in the lungs of mice with emphysema and its effects on the differentiation of CD4+ T cell].

Objective: To evaluate the expression of interleukin (IL)-21 in a cigarette smoke-induced mice model of emphysema and explore its effects on the differentiation of CD4(+)T cell.

Methods: Twenty male Balb/c mice were randomly divided into two groups: control group and smoke-exposed group. Morphological changes were evaluated by mean linear intercepts and alveolar destructive index. The proportion of CD4(+)IL-21R(+)T cells in lungs of mice was determined by flow cytometry. And the levels of IL-21 in lungs of mice were analyzed by enzyme-linked immunosorbent assay (ELISA). Fresh lung mononuclear cells were isolated from the smoke-exposed group and divided further into two sub-groups: blank sub-group and co-culture sub-group. Two sub-groups were cultured in medium with or without IL-21 for 24 h and 48 h. The proportions of Th1 and Th17 cells in cell culture medium were determined by flow cytometry.

Results: Mean linear intercepts and alveolar destructive index in the smoke-exposed group ((48.6 ± 4.8) µm and 44.9 ± 2.8) were significantly higher than the control group ((32.4 ± 4.0) µm and 28.1 ± 2.1, both P < 0.05). In lungs, the percentage of CD4(+)IL-21R(+)T cells in the smoke-exposed group (4.1% ± 1.5%) significantly increased than that in the control group (1.4% ± 0.4%) (P < 0.05). The levels of IL-21 in lung of the smoke-exposed group ((851 ± 28) ng/L) were higher than those in the control group ((415 ± 39) ng/L, P < 0.05). In lungs, the levels of IL-21 had positive correlations with mean linear intercepts and alveolar destructive index (r = 0.892 and 0.955, both P < 0.05). The percentages of Th1 and Th17 cells in cell culture medium of the co-culture sub-group for 24 h and 48 h significantly increased versus those in the blank group (all P < 0.05).

Conclusion: IL-21 may participate in the occurrence and development of emphysema through the induced differentiation of CD4(+)T cells and the promotion of Th1 and Th17-cell responses in lungs.