title: Type 2 rhinovirus infection of cultured human tracheal epithelial cells: role of LDL receptor.
abstract: 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-kappaB (NF-kappaB). 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.
authors.affiliation: Department of Geriatric and Respiratory Medicine, Tohoku University School of Medicine, Sendai 980-8574, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Suzuki
authors.forename: M
authors.initials: M
authors.lastname: Yamaya
authors.forename: M
authors.initials: M
authors.lastname: Kamanaka
authors.forename: Y X
authors.initials: YX
authors.lastname: Jia
authors.forename: K
authors.initials: K
authors.lastname: Nakayama
authors.forename: M
authors.initials: M
authors.lastname: Hosoda
authors.forename: N
authors.initials: N
authors.lastname: Yamada
authors.forename: H
authors.initials: H
authors.lastname: Nishimura
authors.forename: K
authors.initials: K
authors.lastname: Sekizawa
authors.forename: H
authors.initials: H
authors.lastname: Sasaki
mesh_terms: D000368:Aged; D000906:Antibodies / Q000494:pharmacology; D002478:Cells, Cultured; D003139:Common Cold / Q000503:physiopathology* / Q000517:prevention & control; D016207:Cytokines / Q000096:biosynthesis; D004247:DNA / Q000378:metabolism; D004198:Disease Susceptibility; D004847:Epithelial Cells / Q000378:metabolism / Q000821:virology; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000276:immunology / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D016328:NF-kappa B / Q000378:metabolism; D016133:Polymerase Chain Reaction; D012367:RNA, Viral / Q000378:metabolism; D011973:Receptors, LDL / Q000276:immunology / Q000502:physiology*; D012229:Rhinovirus / Q000235:genetics; D016329:Sp1 Transcription Factor / Q000378:metabolism; D014132:Trachea / Q000378:metabolism / Q000473:pathology / Q000821:virology*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D000906:Antibodies; D016207:Cytokines; D007375:Interleukin-1; D016328:NF-kappa B; D012367:RNA, Viral; D011973:Receptors, LDL; D016329:Sp1 Transcription Factor; D014409:Tumor Necrosis Factor-alpha; D004247:DNA