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Suzuki, Tomoko, Mutsuo Yamaya, Masahito Kamanaka, Yu X. Jia, Katsutoshi Nakayama, Masayoshi Hosoda, Norihiro Yamada, Hidekazu Nishimura, Kiyohisa Sekizawa, and Hidetada Sasaki. Type 2 rhinovirus infection of cultured human tracheal epithelial cells: role of LDL receptor. Am J Physiol Lung Cell Mol Physiol 280: L409-L420, 2001.--To examine the role of the low-density lipoprotein (LDL) receptor on minor group human rhinovirus (RV) infection, primary cultures of human tracheal epithelial cells were infected with a minor group (RV2) or a major group (RV14) RV. Viral infection was confirmed by showing with PCR that viral titers in supernatants and lysates from infected cells increased with time. RV2 and RV14 increased expression of mRNA and protein of the LDL receptor on the cells and the cytokine production. RV2 induced activation of transcription factors SP1 and nuclear factor-[Kappa]B (NF-[Kappa]B). An antibody to the LDL receptor inhibited RV2 infection and RV2-induced cytokine production without an effect on RV14 infection and RV14-induced cytokine production. These findings imply that RV2 upregulates LDL receptor expression on airway epithelial cells, thereby increasing susceptibility to minor group RV infection. LDL receptor expression and cytokine production may be mediated, in part, via activation of transcription factors by RV2. These events may be important in airway inflammation after minor group RV infection in asthma. asthma; common cold; airway inflammation; low-density lipoprotein receptor

Suzuki, Tomoko, Mutsuo Yamaya, Kiyohisa Sekizawa, Norihiro Yamada, Katsutoshi Nakayama, Satoshi Ishizuka, Masahito Kamanaka, Tetsushi Morimoto, Yoshio Numazaki, and Hidetada Sasaki. Effects of dexamethasone on rhinovirus infection in cultured human tracheal epithelial cells. Am. J. Physiol. Lung Cell. Mol. Physiol. 278: L560-L571, 2000.--To examine the effects of glucocorticoid on rhinovirus (RV) infection, primary cultures of human tracheal epithelial cells were infected with either RV2 or RV14. Viral infection was confirmed by demonstrating that viral RNA in infected cells and viral titers of supernatants and lysates from infected cells increased with time. RV14 infection upregulated the expression of mRNA and protein of intercellular adhesion molecule-1 (ICAM-1), the major RV receptor, on epithelial cells, and it increased the production of interleukin (IL)-1[Beta], IL-6, IL-8, and tumor necrosis factor-[Alpha] in supernatants. Dexamethasone reduced the viral titers of supernatants and cell lysates, viral RNA of infected cells, and susceptibility of RV14 infection in association with inhibition of cytokine production and ICAM-1 induction. In contrast to RV14 infection, dexamethasone did not alter RV2 infection, a minor group of RVs. These results suggest that dexamethasone may inhibit RV14 infection by reducing the surface expression of ICAM-1 in cultured human tracheal epithelial cells. Glucocorticoid may modulate airway inflammation via reducing the production of proinflammatory cytokines and ICAM-1 induced by rhinovirus infection. asthma; common cold; airway inflammation; intercellular adhesion molecule-1