The association of non-specific chronic inflammation with dendritic cells in a rat model of chronic obstructive pulmonary disease

Abstract

To evaluate the changes in the number and maturation of lung tissue dendritic cells (DCs) and to assess the chronic inflammation in a cigarette smoke-induced COPD model in rats. Thirty male F344 rats were randomly divided into 3 groups (n = 10): a control group, a smoke-exposure group and a smoking cessation group. Rat lung pathomorphological changes were observed by hematoxylin-eosin (HE) stain. Lung tissue CD(11c)(+) DCs, CD(86)(+) DCs and CD(8)(+) T cell numbers were observed by immunohistochemistry method. Flow cytometry was used for detection of CD(11c)(+)/CD(86)(+) DCs and CD(11c)(+)/MHCII(+) DCs proportions. The airway inflammatory pathological score and the mean linear intercept (MLI) obtained from he smoke-exposure group and the smoking cessation group (390 ± 33, 324 ± 28) and [(68 ± 11) µm, (58 ± 9) µm] were higher than those in the control group (56 ± 13) and (36 ± 6) µm (F = 459.85 and 34.03, all P < 0.05). In the smoke-exposure group and the smoking cessation group, the positive rate of CD(11c)(+) DCs [(1.47 ± 0.12)%, (1.30 ± 0.17)%], and the positive rate of CD(86)(+) DCs [(1.26 ± 0.18)%, (1.02 ± 0.08)%] were higher than those in the control group [(0.96 ± 0.08)%, (0.65 ± 0.03)%] (F = 6.55 and 30.26, all P < 0.05), but there was no significant difference between the smoke-exposure group and the smoking cessation group (t = 1.10 and 1.47, all P>0.05). In the smoke-exposure group and the smoking cessation group, CD(8)(+) T positive rate [(2.72 ± 0.15)%, (2.35 ± 0.23)%] was higher than that in the control group [(1.39 ± 0.11)%] (F = 16.07, P < 0.05). CD(11c)(+)/CD(86)(+) DCs and CD(11c)(+)/MHCII(+)DCs percentages [(5.5 ± 0.4)%, (4.8 ± 0.4)%], [(4.2 ± 0.4)%, (3.3 ± 0.3)%] decreased in the smoke-exposure group and the smoking cessation group as compared to the control group [(8.0 ± 0.5)%, (6.1 ± 0.5)%] (F = 14.34 and 12.82, all P < 0.05). There was no significant difference between all the above index from the smoke-exposure group and the smoking cessation group (t = 1.10 and 2.11, all P > 0.05). Cigarette smoke exposure induced increased DCs transmigrated and influenced the maturation of DCs in COPD rats. Even after smoking cessation, non-specific chronic inflammation was still present, suggesting that DCs number and maturation abnormality may be involved in the chronic inflammation of COPD.