Abstract
Human respiratory syncytial virus (RSV) sometimes causes acute and severe lower respiratory tract illness in infants and young children. RSV strongly upregulates proinflammatory cytokines and the platelet-activating factor (PAF) receptor, which is a receptor for Streptococcus pneumoniae, in the pulmonary epithelial cell line A549. Clarithromycin (CAM), which is an antimicrobial agent and is also known as an immunomodulator, significantly suppressed RSV-induced production of interleukin-6, interleukin-8, and regulated on activation, normal T-cell expressed and secreted (RANTES). CAM also suppressed RSV-induced PAF receptor expression and adhesion of fluorescein-labeled S. pneumoniae cells to A549 cells. The RSV-induced S. pneumoniae adhesion was thought to be mediated by the host cell's PAF receptor. CAM, which exhibits antimicrobial and immunomodulatory activities, was found in this study to suppress the RSV-induced adhesion of respiratory disease-causing bacteria, S. pneumoniae, to host cells. Thus, CAM might suppress immunological disorders and prevent secondary bacterial infections during RSV infection.
Highlights
Human respiratory syncytial virus (RSV) is one of the most important infectious agents causing acute lower respiratory tract illness, such as bronchiolitis and pneumonia, in infants and young children [1, 2]
We examined the effect of CAM on cytokine production, platelet-activating factor (PAF) receptor expression, and RSV infection-induced S. pneumoniae adhesion to respiratory epithelial cells
RSV infection to A549 cells was performed at multiplicity of infection (MOI) of 1
Summary
Human respiratory syncytial virus (RSV) is one of the most important infectious agents causing acute lower respiratory tract illness, such as bronchiolitis and pneumonia, in infants and young children [1, 2]. Transcriptional induction of proinflammatory cytokines, chemokines, and interferons is mediated by NF-κB and interferon regulatory factors (IRFs) [5, 6] These mediators are believed to contribute to the pathophysiology of RSV infection, such as mucous hypersecretion, swelling of submucous, and infiltration of lymphocytes, neutrophils, eosinophils, and macrophages [7]. S. pneumoniae and H. influenzae colonize to the host respiratory epithelium via host cell surface receptors, such as the platelet-activating factor (PAF) receptor [12,13,14] These bacteria interact with the PAF receptor via phosphorylcholine, which is a component of the bacterial cell surface. Both live and heat-killed S. pneumoniae cells show an increased adhesion to human epithelial cells infected with RSV [15]. The upregulation of PAF receptor expression that is induced by respiratory virus infections, including those caused by RSV, results in the enhanced
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