Expression of IL-6, IL-8, and RANTES on human bronchial epithelial cells, NCI-H292, induced by influenza virus A.
Bronchial epithelial cells are primary sites of airway viral infection, and these cells may play an important role in the pathogenesis of respiratory diseases. It has recently been reported that bronchial epithelial cells express RANTES. RANTES attracts monocytes, T cells, eosinophils, and basophils; it can also activate eosinophils. To determine whether viral infection induces RANTES expression on bronchial epithelial cells, we infected a bronchial epithelial cell line, NCI-H292, with influenza virus A (H3N2). We then examined the concentration of RANTES in the culture medium of infected cells by ELISA and assessed expression of the gene for RANTES by the reverse-transcriptase polymerase chain reaction. We also investigated the concentrations of IL-6, IL-8, and granulocyte-macrophage colony-stimulating factor in the medium of infected cells, because some virus infections have been reported to induce expression of these cytokines on bronchial epithelial cells, but there are few data concerning influenza virus infection. Small amounts of IL-6 and IL-8 were detected in the medium of uninfected cells. RANTES was not detected in the medium of uninfected cells. After influenza virus infection, significant amounts of IL-6, IL-8, and RANTES were released into the culture medium of infected cells, and RANTES messenger RNA was detected from infected cells. Granulocyte-macrophage colony-stimulating factor was not detected in the medium of uninfected and infected cells. These results suggest that influenza virus infection may stimulate production of IL-6, IL-8, and RANTES from human bronchial epithelial cells and that these cytokines may contribute to the pathogenesis of airway inflammatory diseases caused by influenza virus infection.
Matsukura
S
S
First Department of Internal Medicine, University of Showa School of Medicine, Tokyo, Japan.
Kokubu
F
F
Noda
H
H
Tokunaga
H
H
Adachi
M
M
D001483:Base Sequence / Q000235:genetics; D001980:Bronchi / Q000166:cytology / Q000378:metabolism* / Q000821:virology*; D002460:Cell Line; D018946:Chemokine CCL5 / Q000096:biosynthesis* / Q000235:genetics; D004848:Epithelium / Q000378:metabolism / Q000821:virology; D006801:Humans; D009980:Influenza A virus / Q000302:isolation & purification* / Q000472:pathogenicity*; D015850:Interleukin-6 / Q000096:biosynthesis*; D016209:Interleukin-8 / Q000096:biosynthesis*; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D012367:RNA, Viral / Q000032:analysis
D018946:Chemokine CCL5; D015850:Interleukin-6; D016209:Interleukin-8; D012333:RNA, Messenger; D012367:RNA, Viral