Key result
Bafilomycin A1 reduced rhinovirus 14 viral titers and inhibited the production of cytokines and ICAM-1 in human airway epithelial cells.
Why the study?
Does bafilomycin A1 inhibit rhinovirus infection in human airway epithelium?
Does bafilomycin A1 inhibit rhinovirus infection in human airway epithelium?
Bafilomycin A1 inhibits rhinovirus infection in human airway epithelial cells by blocking viral RNA entry into endosomes and reducing ICAM-1 expression.
Answers are grounded in this paper and cite their sources.
Bafilomycin A1 merits in vivo testing; leaves open therapeutic utility in rhinovirus airway disease.
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 infection was 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 the viral titers of RV14 and inhibited the production of cytokines and ICAM-1 before and after RV14 infection. Bafilomycin A(1) reduced susceptibility of epithelial 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.
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Suzuki et al. (2001) studied Rhinovirus infection. Bafilomycin A1 was evaluated on Viral titers, cytokine production, and ICAM-1 expression. Bafilomycin A1 reduced rhinovirus 14 viral titers and inhibited the production of cytokines and ICAM-1 in human airway epithelial cells.
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