TY - JOUR
T1 - Modulation of respiratory syncytial virus-induced prostaglandin E 2 production by n-3 long-chain polyunsaturated fatty acids in human respiratory epithelium
AU - Bryan, Dani Louise
AU - Hart, Prue
AU - Forsyth, Kevin
AU - Gibson, Robert
N1 - Funding Information:
This work was supported by grants from the Australian Research Council and Goodman Fielder Ltd. R.G. was partly supported by the MS McLeod Research Trust; P.H. was partly supported by the National Health and Medical Research Council. The authors thank Mark Neumann for statistical and technical assistance.
PY - 2005/10
Y1 - 2005/10
N2 - Infection with respiratory syncytial virus (RSV) results in substantial infant morbidity and has been associated with the subsequent development of childhood asthma. Inflammatory mediators produced by both the epithelium and tissue leukocytes during RSV infection stimulate the release of chemotactic factors by the respiratory epithelium and the subsequent influx of inflammatory cells, predominantly neutrophils. We investigated the production of inflammatory mediators [prostaglandin E 2 (PGE 2), interleukin (IL)-1β, tumor necrosis factor a] and chemokines [IL-8, RANTES (regulation on activation, normal T cell expressed and secreted)] by alveolar epithelial cells in response to RSV infection. Infection of a human alveolar epithelial transformed cell line (A549 cells) with live RSV substantially increased production of PGE 2, IL-8, and RANTES. By altering cell membrane FA through incorporation of the long-chain PUFA (LCPUFA) arachidonic acid, EPA, and DHA, we were subsequently able to significantly modulate PGE 2 production by the infected epithelium. Because of the dynamic nature of the effects of PGE 2 on lung function, regulation of this prostaglandin during RSV infection by n-3 LCPUFA has the potential to significantly alter the disease process.
AB - Infection with respiratory syncytial virus (RSV) results in substantial infant morbidity and has been associated with the subsequent development of childhood asthma. Inflammatory mediators produced by both the epithelium and tissue leukocytes during RSV infection stimulate the release of chemotactic factors by the respiratory epithelium and the subsequent influx of inflammatory cells, predominantly neutrophils. We investigated the production of inflammatory mediators [prostaglandin E 2 (PGE 2), interleukin (IL)-1β, tumor necrosis factor a] and chemokines [IL-8, RANTES (regulation on activation, normal T cell expressed and secreted)] by alveolar epithelial cells in response to RSV infection. Infection of a human alveolar epithelial transformed cell line (A549 cells) with live RSV substantially increased production of PGE 2, IL-8, and RANTES. By altering cell membrane FA through incorporation of the long-chain PUFA (LCPUFA) arachidonic acid, EPA, and DHA, we were subsequently able to significantly modulate PGE 2 production by the infected epithelium. Because of the dynamic nature of the effects of PGE 2 on lung function, regulation of this prostaglandin during RSV infection by n-3 LCPUFA has the potential to significantly alter the disease process.
UR - https://www.scopus.com/pages/publications/33644875367
U2 - 10.1007/s11745-005-1463-4
DO - 10.1007/s11745-005-1463-4
M3 - Article
C2 - 16382572
AN - SCOPUS:33644875367
SN - 0024-4201
VL - 40
SP - 1007
EP - 1011
JO - Lipids
JF - Lipids
IS - 10
ER -