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Medium‐chain fatty acids stimulate interleukin‐8 production in Caco‐2 cells with different mechanisms from long‐chain fatty acids 1
Author(s) -
Tanaka Seigou,
Saitoh Osamu,
Tabata Kazue,
Matsuse Ryoichi,
Kojima Keishi,
Sugi Kazunori,
Nakagawa Ken,
Kayazawa Masanobu,
Teranishi Tsutomu,
Uchida Kazuo,
Hirata Ichiro,
Katsu KenIchi
Publication year - 2001
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.2001.02537.x
Subject(s) - calphostin , calphostin c , docosahexaenoic acid , protein kinase c , eicosapentaenoic acid , interleukin 8 , caco 2 , oleic acid , biochemistry , protein kinase a , microbiology and biotechnology , fatty acid , kinase , chemistry , medicine , biology , polyunsaturated fatty acid , cytokine , cell
Background and Aim: It has been suggested that dietary fat exacerbates intestinal inflammation. We investigated the effect of fatty acids on interleukin (IL)‐8 production in a human intestinal epithelial cell line (Caco‐2). Methods: The cells were cultured as monolayers on microporous membranes in culture inserts. Oleic acid (OA), capric acid (CA), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) were applied to the apical compartment of Caco‐2 cell monolayers. The concentration of IL‐8 in the basolateral medium was measured by using enzyme‐linked immunosorbent assay, and the expression of IL‐8 mRNA was measured by using competitive reverse transcription–polymerase chain reaction. Protein kinase C inhibitors (GF109203X and calphostin C) and H‐7 (a protein kinase inhibitor) were used to study the mechanisms by which IL‐8 production is stimulated. Results: Both OA and CA enhanced IL‐8 production (approximately fivefold), whereas DHA and EPA did not. Both OA and CA also enhanced IL‐1‐induced IL‐8 production. The onset of OA‐induced IL‐8 production was delayed compared with that of CA‐induced IL‐8 production. Both OA and CA enhanced IL‐8 mRNA expression (approximately fivefold) after 6 and 3 h, respectively. The protein kinase inhibitor (H‐7) reduced both OA‐ and CA‐induced IL‐8 production by 88.0 and 85.9%, respectively. The protein kinase C inhibitors (GF109203X and calphostin C) reduced OA‐induced IL‐8 production by 29.3 and 54.5%, respectively, but showed no effect on CA‐induced IL‐8 production. Conclusions: These findings suggest that not only OA but also CA stimulates IL‐8 production in intestinal epithelial cells, and the mechanisms of action differ between OA and CA.