Cytokine induction by respiratory syncytial virus and adenovirus in bronchial epithelial cells

Abstract

In order to broaden our knowledge of the primary immune responses to respiratory syncytial virus (RSV) and adenovirus infections, we compared the concentrations of interleukin (IL)-6, IL-8, and regulated on activation, normal T cell expressed and secreted (RANTES) produced in vitro during RSV and adenovirus infections of bronchial epithelial cells. We infected BEAS-2B cells-a human bronchial epithelial cell line-with RSV, adenovirus serotype 3, or serotype 7 and measured the concentrations of IL-6, IL-8, and RANTES in the cell culture supernatants. When the multiplicity of infection (MOI) was 1, RSV induced the production of markedly higher concentrations of IL-6, IL-8, and RANTES than the adenovirus. When the MOI of the adenovirus was increased to 100, the production of IL-6 and IL-8 increased. However, the amounts produced were still lower than those produced by RSV with the MOI of 1. There was no statistically significant increase in the production of RANTES in spite of the MOI of the adenovirus was increased to 100. Adenovirus serotype 7 induced the production of considerably more IL-6 and IL-8 than serotype 3 in the MOI of 100. However, neither adenovirus serotype triggered an increase in the production of RANTES in spite of the MOI of 100. This demonstrates that RSV could have a superior capacity to stimulate the production of IL-6, IL-8, and RANTES in the bronchial epithelial cells. This study may help to explain the differences in the clinical outcomes of RSV and adenovirus infections.

Lack of an exaggerated inflammatory response on virus infection in cystic fibrosis

“…The airway epithelial inflammatory response towards respiratory viruses is of considerable variability and depends, among other factors, on virus type, strain and load, cell culture conditions and infected cell type [32][33][34]. Thus, data obtained from only a single in vitro model system should be interpreted with caution.…”

Lipopolysaccharide Induces IL-6 Production in Respiratory Syncytial Virus-Infected Airway Epithelial Cells Through the Toll-Like Receptor 4 Signaling Pathway

“…Endotoxin, or its purified derivative LPS, a cell wall component of Gramnegative bacteria, is a potent proinflammatory constituent continuously shedding into the environment, which is important in the pathogenesis of airway inflammatory diseases such as asthma. To study whether LPS-induced cytokine or chemokine production in noninfected airway epithelial cells, we chose chemokine CXC family member IL-8, IL-6 cytokine and the chemokine CCL family member RANTES as examples, as they also play a pivotal role in airway immune response to RSV infection (15,19). We found that incubation with 50 g/mL LPS (the dose choosing data were not shown) slightly up-regulated IL-6 production in 9HTEo cells (Fig.…”

Fosfomycin Suppresses Chemokine Induction in Airway Epithelial Cells Infected with Respiratory Syncytial Virus

“…IL-8 primarily targets the neutrophil and promotes neutrophil migration to the site of inflammation. It is suggested that neutrophils induced by IL-8 inflammation play an important role during airway RSV infection (37). RANTES and IL-8 induced by RSV infection activate the release of leukotrienes and histamine in primed mast cells and basophils (2,4).…”