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Modulation of respiratory syncytial virus‐induced prostaglandin E 2 production by n−3 long‐chain polyunsaturated fatty acids in human respiratory epithelium
Author(s) -
Bryan DaniLouise,
Hart Prue,
Forsyth Kevin,
Gibson Robert
Publication year - 2005
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/s11745-005-1463-4
Subject(s) - respiratory epithelium , prostaglandin e , chemokine , prostaglandin e2 , biology , epithelium , immunology , arachidonic acid , leukotriene b4 , respiratory system , immune system , inflammation , endocrinology , biochemistry , genetics , enzyme , anatomy
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 α] 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.