Tl. Noah et S. Becker, RESPIRATORY SYNCYTIAL VIRUS-INDUCED CYTOKINE PRODUCTION BY A HUMAN BRONCHIAL EPITHELIAL-CELL LINE, The American journal of physiology, 265(5), 1993, pp. 120000472-120000478
Respiratory syncytial virus (RSV) is the most common cause of lower re
spiratory infection in infants and young children, but the pathogenesi
s of RSV-induced inflammation is not well defined. We hypothesized tha
t in vitro infection of a human bronchial epithelial cell line (BEAS)
would induce production of proinflammatory cytokines. BEAS cells were
infected with RSV, and cells and supernatants were assayed for cytokin
e mRNA and protein changes at several time points after infection. Cyt
okine mRNA in BEAS cells was measured by polymerase chain reaction of
reverse-transcribed RNA from whole cell lysates; cytokine levels in su
pernatants were measured by bioassay or immunoassay. Our results indic
ated that interleukin-8 (IL-8) was induced at 4 h after infection (dur
ing the eclipse phase of RSV infection) with accumulation of IL-8 in s
upernatants by 24 h after infection. Increased levels of IL-6 and gran
ulocyte macrophage colony-stimulating factor in supernatants were only
detected by 96 h after infection, during the RSV replicative phase. I
nterferon-alpha and -gamma transcripts were not detectable at any time
point. We conclude that the effects of RSV on airway inflammation may
be at least partly mediated by sequential production of proinflammato
ry cytokines in infected airway epithelium.