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Titolo:
Bafilomycin A(1) inhibits rhinovirus infection in human airway epithelium:effects on endosome and ICAM-1
Autore:
Suzuki, T; Yamaya, M; Sekizawa, K; Hosoda, M; Yamada, N; Ishizuka, S; Nakayama, K; Yanai, M; Numazaki, Y; Sasaki, H;
Indirizzi:
Tohoku Univ, Sch Med, Dept Geriatr & Resp Med, Aoba Ku, Sendai, Miyagi 9808574, Japan Tohoku Univ Sendai Miyagi Japan 9808574 Ku, Sendai, Miyagi 9808574, Japan Sendai Natl Hosp, Div Clin Res, Virus Ctr, Sendai, Miyagi 9830045, Japan Sendai Natl Hosp Sendai Miyagi Japan 9830045 endai, Miyagi 9830045, Japan Univ Tsukuba, Inst Clin Med, Dept Pulm Med, Tsukuba, Ibaraki 3058575, Japan Univ Tsukuba Tsukuba Ibaraki Japan 3058575 sukuba, Ibaraki 3058575, Japan
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 6, volume: 280, anno: 2001,
pagine: L1115 - L1127
SICI:
1040-0605(200106)280:6<L1115:BAIRII>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
ADHESION MOLECULE-1 ICAM-1; INTRACELLULAR PH; NA+/H+ EXCHANGE; PROTON PUMP; IN-VIVO; CELLS; ACIDIFICATION; EXPRESSION; RECEPTOR; VIRUSES;
Keywords:
intercellular adhesion molecule-1; asthma; common cold; airway inflammation; vacuolar adenosine 5 '-triphosphatase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Sasaki, H Tohoku Univ, Sch Med, Dept Geriatr & Resp Med, Aoba Ku, Seiryo Machi 1-1, Sendai, Miyagi 9808574, Japan Tohoku Univ Seiryo Machi 1-1 SendaiMiyagi Japan 9808574 , Japan
Citazione:
T. Suzuki et al., "Bafilomycin A(1) inhibits rhinovirus infection in human airway epithelium:effects on endosome and ICAM-1", AM J P-LUNG, 280(6), 2001, pp. L1115-L1127

Abstract

To examine the effects of bafilomycin A(1), a blocker of vacuolar H+-ATPase, on rhinovirus (RV) infection in the airway epithelium, primary cultures of human tracheal epithelial cells were infected with RV14. Viral infectionwas confirmed by showing that viral RNA in the infected cells and the viral titers in the supernatants of infected cells increased with time. RV14 infection upregulated the production of cytokines and mRNA of intercellular adhesion molecule (ICAM)-1 in epithelial cells. Bafilomycin A(1) reduced theviral titers of RV14 and inhibited the production of cytokines and ICAM-1 before and after RV14 infection. Bafilomycin A(1) reduced susceptibility ofepithelial cells to RV14 infection. RV14 increased activated nuclear factor-kappaB in the cells, and bafilomycin A(1) reduced the activated nuclear factor-kappaB. Bafilomycin A(1) decreased the number of acidic endosomes in the epithelial cells. These results suggest that bafilomycin A(1) may inhibit infection by RV14 by not only blocking RV RNA entry into the endosomes but also reducing ICAM-1 expression in the epithelial cells. Bafilomycin A(1) may therefore modulate airway inflammation after RV infection.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 18:29:06