Objective: To investigate the changes and of nuclear factor-kappa B (NF-kappaB) and intercellular adhesion molecule (ICAM)-1 expression in airway epithelial cells from smoking rats.
Methods: Wistar rats (n = 39) were randomly divided into a nonsmoking control group and 2 smoking groups-smoking for 1 month and 3 months, with 13 rats in each group. Immunohistochemistry and in situ hybridization staining were used to semiquantitatively analyse the changes of NF-kappaB and ICAM-1 expression in airway epithelial cells.
Results: (1) The percentages of positive cells for NF-kappaB nuclear staining in bronchiolar epithelial cells in 1 month smoking group (63 +/- 4)% and 3 month smoking group [(51 +/- 5)%] were significantly higher than that in the control group [(27 +/- 5)%] (P < 0.01 respectively). (2) ICAM-1 mRNA expression in bronchial and bronchiolar epithelial cells in the 1 month smoking group (0.645 +/- 0.038, 0.747 +/- 0.041) and the 3 month smoking group (0.688 +/- 0.062, 0.809 +/- 0.023) was significantly higher than those in the control group (0.526 +/- 0.023, 0.635 +/- 0.044), (P < 0.01 respectively), and the expression of ICAM-1 mRNA in the 3 month smoking group was higher than that in the 1 month smoking group (P < 0.05 and P < 0.01 respectively). (3) ICAM-1 protein expression in the main bronchial and bronchiolarepithelial cells in the 1 month smoking group (0.73 +/- 0.04, 0.94 +/- 0.05) and the 3 month smoking group (0.77 +/- 0.04, 0.99 +/- 0.03) was significantly higher than those in the control group (0.57 +/- 0.04, 0.83 +/- 0.04) (P < 0.01 respectively), and the expression of ICAM-1 protein in the 3 month smoking group was higher than those in the 1 month smoking group (P < 0.05 respectively). (4) ICAM-1 mRNA and protein expression in bronchioles were significantly higher than those in the bronchi (P < 0.01 respectively) in all groups. (5) The percentage of cells staining positive for nuclear NF-kappaB correlated with ICAM-1 protein expression in bronchioles from the 1 month smoking group (r = 0.462, P < 0.05).
Conclusion: NF-kappaB and ICAM-1 may play an important role in smoking-induced airway inflammation.