Journal
CELL BIOLOGY INTERNATIONAL
Volume 37, Issue 4, Pages 326-339Publisher
WILEY
DOI: 10.1002/cbin.10044
Keywords
cytokine; fluticasone propionate; human foetal lung fibroblast; respiratory syncytial virus; signalling pathway
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Funding
- Ministry of Health, Labour and Welfare, Japan
- Grants-in-Aid for Scientific Research [23591470] Funding Source: KAKEN
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To examine cytokine production in response to RSV infection, we assessed the levels of 29 cytokines released from RSV-infected human foetal lung fibroblasts. We also examined the relationships between the effects of fluticasone propionate and various signalling pathways in the cells. Twenty-four hours after infection (1MOI), RSV-infected cells released cytokines, for example proinflammatory cytokines (IL-1, IL-6 and TNF-), anti-inflammatory (IL-1ra), Th1 (IFN-, IFN-1a, IL-2 and IL-12), Th2 (IL-4, IL-5, IL-10 and IL-13), granulopoiesis-inducing (G-CSF and GM-CSF), eosinophil recruitment-inducing (eotaxin and RANTES) and neutrophil recruitment-inducing cytokines (IL-8, IP-10, MCP-1 and MIP-1). Aberrant release of most was significantly suppressed by fluticasone propionate. Twelve hours after RSV infection, increased phosphorylation of Akt, p38 MAPK, ERK1/2 and IB- was noted. Fluticasone propionate suppressed the phosphorylation of Akt, p38 MAPK, and ERK1/2, but not IB-, in virus-infected cells. TLR-4 expression was unchanged in control and RSV-infected cells, and TLR-3 and RIG-I expression was not detected. The results indicate that RSV infection induces aberrant production and release of certain cytokines through these signalling pathways in human lung fibroblasts. Overproduction and imbalance of these cytokines may be associated with the pathophysiology of RSV-induced excessive and allergic inflammation.
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