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Titolo:
RHINOVIRUS INFECTION OF PRIMARY CULTURES OF HUMAN TRACHEAL EPITHELIUM- ROLE OF ICAM-1 AND IL-1-BETA
Autore:
TERAJIMA M; YAMAYA M; SEKIZAWA K; OKINAGA S; SUZUKI T; YAMADA N; NAKAYAMA K; OHRUI T; OSHIMA T; NUMAZAKI Y; SASAKI H;
Indirizzi:
TOHOKU UNIV,SCH MED,DEPT GERIATR MED,AOBA KU,SEIRYO MACHI 1-1 SENDAI MIYAGI 980 JAPAN TOHOKU UNIV,SCH MED,DEPT GERIATR MED,AOBA KU SENDAI MIYAGI 980 JAPAN SENDAI NATL HOSP,DIV CLIN RES,VIRUS CTR SENDAI MIYAGI 983 JAPAN
Titolo Testata:
American journal of physiology. Lung cellular and molecular physiology
fascicolo: 4, volume: 17, anno: 1997,
pagine: 749 - 759
SICI:
1040-0605(1997)17:4<749:RIOPCO>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERCELLULAR-ADHESION MOLECULE-1; RESPIRATORY SYNCYTIAL VIRUS; TUMOR-NECROSIS-FACTOR; COMPLEMENTARY-DNA; CELL LINE; EXPRESSION; CLONING; CDNA; INTERLEUKIN-1; ASTHMA;
Keywords:
ASTHMA; COMMON COLD; AIRWAY INFLAMMATION; INTERLEUKIN-1-BETA; INTERCELLULAR ADHESION MOLECULE-1; POLYMERASE CHAIN REACTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
35
Recensione:
Indirizzi per estratti:
Citazione:
M. Terajima et al., "RHINOVIRUS INFECTION OF PRIMARY CULTURES OF HUMAN TRACHEAL EPITHELIUM- ROLE OF ICAM-1 AND IL-1-BETA", American journal of physiology. Lung cellular and molecular physiology, 17(4), 1997, pp. 749-759

Abstract

Exacerbations of asthma are often associated with respiratory infection caused by rhinoviruses. To study the effects of rhinovirus infection on respiratory epithelium, a primary target for respiratory viruses,human rhinovirus (HRV)-2 and HRV-14 were infected to primary culturesof human tracheal epithelial cells. Viral infection was confirmed by showing that viral titers of supernatants and lysates from infected cells increased with time and by polymerase chain reaction. HRV-8 and HRV-14 infections upregulated the expression of intercellular adhesion molecule-1 (ICAM-1) mRNA, the major rhinovirus receptor, on epithelial cells, and they increased the production of interleukin (IL)-1 beta, IL-6, IL-8, and tumor necrosis factor (TNF)-alpha in supernatants. Antibodies to ICAM-1 inhibited HRV-14 infection of epithelial cells and decreased the production of cytokines after HRV-14 infection, but they did not alter HRV-2 infection-induced production of cytokines. IL-1 beta upregulated ICAM-1 mRNA expression and increased susceptibility to HRV-14 infection, whereas other cytokines failed to alter ICAM-1 mRNA expression. Furthermore, a neutralizing antibody to IL-1 beta significantly decreased viral titers of supernatants and ICAM-1 mRNA expressionafter HRV-14 infection, but a neutralizing antibody to TNF-alpha was without effect. Immunohistochemical studies revealed that both HRV-14 infection and IL-1 beta increased ICAM-1 expression on cultured epithelial cells. These findings imply that HRV-14 infection upregulated ICAM-1 expression on epithelial cells through increased production of IL-1 beta, thereby increasing susceptibility to infection. These events may be important for amplification of airway inflammation after viral infection in asthma.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/08/20 alle ore 05:35:27