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*
First Department of Internal Medicine and
Department of Microbiology, Nihon University School of Medicine, Tokyo, Japan
Airway epithelial cells which are the initial site of influenza
virus (IV) infection are suggested to participate in airway
inflammatory response by expressing various cytokines including RANTES;
however, the intracellular signal that regulates RANTES expression has
not been determined. In the present study, we examined the role of p38
mitogen-activated protein (MAP) kinase, extracellular signal-regulated
kinase (Erk), and c-Jun-NH2-terminal kinase (JNK) in RANTES
production by IV-infected human bronchial epithelial cells. The results
showed that IV infection induced increases in p38 MAP kinase, and Erk
and JNK phosphorylation and activity. SB 203580, PD 98059, and CEP-1347
attenuated IV-infection induced p38 MAP kinase activity, Erk activity,
and JNK activity, respectively. SB 203580 and CEP-1347 attenuated
RANTES production by 45.3% and 45.2%, respectively, but a combination
of these inhibitors additively attenuated by 69.1%. In contrast, PD
98059 did not attenuate. Anti-IL-1
mAb, anti-IL-1ß mAb,
anti-TNF- mAb, anti-IL-8 mAb, anti-IFN-ß mAb,
anti-RANTES mAb, and a combination of these mAbs did not affect IV
infection-induced increases in p38 MAP kinase, Erk, and JNK
phosphorylation, indicating that each cytokine neutralized by
corresponding Ab was not involved in IV infection-induced
phosphorylation of MAP kinases. N-acetylcysteine (NAC)
did not affect IV infection-induced increases in MAP kinase
phosphorylation, whereas NAC attenuated RANTES production by 18.2%,
indicating that reactive oxygen species may act as a second messenger
leading to RANTES production via p38 MAP kinase- and JNK-independent
pathway. These results indicate that p38 MAP kinase and JNK, at least
in part, regulate RANTES production by bronchial epithelial
cells.
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