Objective: To investigate the effect of cigarette
smoke exposure on the expression of
CC Chemokine receptor 7 (CCR7) and levels of Th1/Th2
cytokines in asthmatic rats. Methods: Forty Wistar rats were randomly divided into four groups: control group,
asthma group,
smoke exposure group,
asthma-
smoke exposure group. The
asthma group were sensitized with
ovalbumin (OVA) and
Aluminum hydroxide at day 1, 8 and challenged with OVA at day 15 by atomization for 8 weeks.While control group was sensitized and challenged with
normal saline instead of OVA.The
smoke exposure group was sensitized and challenged with
normal saline instead of OVA followed
passive smoking for 8 weeks. The
asthma-
smoke exposure group was challenged with OVA followed
passive smoking. The pathological changes of different groups were observed by HE-staining. CCR7 was semiquantitatively analyzed in lungs by immunohistochemistry.The concentration of
CC chemokine ligand (CCL)19, CCL21,
interferon (IFN)-γ and
interleukin (IL)-4 in peripheral blood and CCL19 and CCL21 in bronchoalveolar lavage fluid (BALF) were measured by
enzyme-linked
immunosorbent (ELESA) assay. Results: In
asthma group,
smoke exposure group and
asthma-
smoke exposure group, the various degrees of inflammatory reaction appeared in lung tissue and the
asthma-
smoke exposure group was with the most significant reaction. In the lung tissues of the rats from
asthma group,
smoke exposure group and
asthma-
smoke exposure group, the average optical density (AOD) of CCR7 were significantly higher than those in control group (0.350±0.023, 0.252±0.022, 0.400±0.029 vs 0.180±0.020, all P<0.01). The AOD of CCR7 of
asthma-
smoke exposure group was much higher than both that in
asthma group and in
smoke exposure group (both P<0.01). In
asthma group,
smoke exposure group and
asthma-
smoke exposure group, the concentrations of both CCL19 and CCL21 in peripheral blood and BALF were significantly higher than that in control group (all P<0.01). The concentrations of both CCL19 and CCL21 in peripheral blood and BALF of
asthma-
smoke exposure group were significantly higher than the results in
asthma group and in
smoke exposure group (all P<0.01). The concentrations of IFN-γ in peripheral blood of
asthma group and
asthma-
smoke exposure group were lower than those in control group [(33±3), (17±3) vs (70±4) pg/ml], but
asthma-
smoke exposure group was much lower than the results in
asthma group (all P<0.01). The concentration of IFN-γ in peripheral blood of
smoke exposure group[(100±5)pg/ml]was higher than that in control group and
asthma-
smoke exposure group (both P<0.01). In
asthma group,
smoke exposure group,
asthma-
smoke exposure group, the concentrations of
IL-4 in peripheral blood were significantly higher than those in control group [(54±4), (42±4), (76±4) vs (30±4) pg/ml, all P<0.01]. The concentrations of
IL-4 in peripheral blood of
asthma-
smoke exposure group was significantly higher than those in
asthma group and in
smoke exposure group (both P<0.01). Conclusion: Cigarette
smoke could enhance the expression of CCR7 and its
ligand, and it can also result in exacerbations of
asthma by reducing the expression level of IFN-γ (the representative of Th1
cytokine) and increasing the expression level of
IL-4 (the representative of Th2
cytokine).