Respiratory syncytial virus (RSV) is a negative-sense, single-strand RNA virus that can initiate severe
bronchiolitis in infants, as well as in elderly adults. Although RSV preferentially infects and replicates in the airway epithelium, studies have shown that RSV has the ability to infect and, to a limited extent, replicate in alveolar macrophages. In the present study, we sought to characterize the RSV-induced
chemokine production in vitro and in vivo, because
chemokines have been shown to contribute to both the
inflammation and pathophysiology of disease. Our results show that RSV-infected airway epithelial cells and alveolar macrophages display differential profiles of
chemokine production: airway epithelial cells produce CCL2/
monocyte chemoattractant protein-1, CCL5/
RANTES, CXCL10/
gamma interferon inducible protein-10, and kerotinocyte
cytokine (KC); and alveolar macrophages up-regulate CCL5 and
macrophage inflammatory protein (MIP)-2 after
RSV infection. In vivo, we observed the induction of CCL2, CCL3/MIP-1 alpha, CCL5, CXCL10, and KC after
RSV infection. In the present study, we also addressed the necessity for
viral infection and/or replication in
chemokine induction by use of ultraviolet (UV)-inactivated RSV, as well as RSV inhibitors of binding/
infection and replication, that is, NMSO3, a sulfated sialyl
lipid compound, and
ribavirin, respectively. Our results suggest that viral replication is necessary for optimal
chemokine production.