Objective: To explore the effects of early cigarette smoke exposure on the immune functions of T-lymphocyte subsets in asthmatic mice model.
Methods: Forty mice (20 days) were randomly allocated into four groups: air control group, cigarette smoke (CS) control group, air+ovalbumin (OVA) group, and CS+OVA group (n = 10 each). The CS control and CS+OVA groups were exposed to cigarette smoke for 3 weeks while the other two groups exposed to air. At an age of 8 weeks, air+OVA and CS+OVA groups had OVA sensitization for establishing an asthma model while the other two groups were selected as control. The percentage of regulatory T cells (Treg), effect of T cell (Te) subgroup including T helper type (Th)1, Th2 and Th17 in splenic mononuclear T cell were determined by flow cytometry. The levels of transforming growth factor-β (TGF-β), interleukin (IL)-4, IL-5, IL-10, IL-13, IL-17A and interferon-γ (IFN-γ) in bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immunosorbent assay (ELISA). And the percentage ratios of Treg to Te were compared among four groups.
Results: The percentages of Th1, Th2, Th17 and Treg in splenic mononuclear of CS+OVA group ((21.47 ± 2.84)%, (16.33 ± 3.02)%, (1.89 ± 0.23)% and (2.92 ± 0.40)%, respectively) were all significantly higher than those in air+OVA group ((14.78 ± 2.21)%, (9.72 ± 1.46)%, (1.01 ± 0.12)% and (1.84 ± 0.22)% , respectively), the levels of IL-4, IL-5, IL-10, IL-13, IL-17A, IFN- γ and TGF-β in BALF of CS+OVA group ((138.6 ± 18.9), (195.3 ± 32.6), (22.8 ± 3.9), (716.9 ± 123.6), (62.8 ± 7.9), (173.2 ± 25.5) and (66.5 ± 8.2) ng/L, respectively) were all significantly higher than those in air+OVA group ((90.1 ± 13.7), (128.5 ± 21.8), (14.4 ± 2.9), (421.4 ± 60.4), (40.4 ± 6.2), (113.8 ± 16.9) and (42.9 ± 3.8) ng/L, respectively) (all P < 0.05). No significant difference of Treg/Te percentage ratio existed in mice spleen mononuclear cells between air+OVA group and CS+OVA group (P > 0.05).
Conclusion: Early cigarette smoke exposure could significantly exacerbate T cell immune dysfunction in asthmatic mice.