RESPIRATORY SYNCYTIAL VIRUS-INFECTION ENHANCES NEUTROPHIL AND EOSINOPHIL ADHESION TO CULTURED RESPIRATORY EPITHELIAL-CELLS - ROLES OF CD18 AND INTERCELLULAR-ADHESION MOLECULE-1
J. Stark et al., RESPIRATORY SYNCYTIAL VIRUS-INFECTION ENHANCES NEUTROPHIL AND EOSINOPHIL ADHESION TO CULTURED RESPIRATORY EPITHELIAL-CELLS - ROLES OF CD18 AND INTERCELLULAR-ADHESION MOLECULE-1, The Journal of immunology, 156(12), 1996, pp. 4774-4782
Respiratory syncytial virus (RSV) infections in children precipitate a
cute episodes of respiratory obstruction that are associated with infl
ux of inflammatory cells into the airway. Since RSV can induce the exp
ression of adhesion molecules, particularly intercellular adhesion mol
ecule-1 (ICAM-1), by the respiratory epithelium, the hypothesis has be
en proposed that ICAM-1 expression contributes to airway inflammation
by supporting adhesion and retention of infiltrating inflammatory leuk
ocytes. To test this hypothesis, A549 cells (an immortalized human alv
eolar epithelial type II cell-like line) were infected with RSV, and t
he ability of these infected monolayers to support adhesion by human n
eutrophils (NEUT) and eosinophils (EOS) was measured. RSV infection si
gnificantly increased ICAM-1 expression by A549 monolayers (p < 0.001)
. Although NEUT adhesion to A549 monolayers was significantly enhanced
following RSV infection (p < 0.001), infection alone resulted in litt
le change in EOS adherence, However, if EOS were first activated with
phorbol ester (PMA), adhesion to both control and RSV-infected A549 ce
lls was enhanced, with greater levels of adhesion supported by RSV-inf
ected cultures (p < 0.001), The requirement for EOS activation (but no
t for NEUT activation) before adhesion remained when NEUT and EOS were
prepared and compared from the same donor. Despite this difference, N
EUT and EOS adhesion was reduced by blocking Abs to epithelial ICAM-1
or granulocyte CD18 adhesion proteins (p < 0.01), However, only NEUT a
dhesion was blocked by Ab to CD11a, Our results show that RSV infectio
ns of respiratory epithelial monolayers can promote inflammatory cell
adherence which could, in turn, potentially contribute to the airway i
njury and obstruction that accompanies bronchiolitis.