Evidence supporting an enhanced consumption of long-chain n-3 PUFAs includes a study in which children with atopic eczema were found to have lower serum levels of EPA and DHA than non-atopic children, despite similar levels of fish consumption [2]. Results from intervention

studies have been inconclusive [13–15]. Various animal models have been used to study the role of n-3 PUFAs in atopic inflammation. Yokoyama et al. [16] showed a reduced atopic asthma reaction in a mouse model after exposure to aerosolized DHA. Yoshino and Ellis [17] reported a tendency towards reduced cell-mediated hypersensitivity reactions in mice fed a fish oil-supplemented diet. However, neither study Adriamycin in vivo noted any effect on IgE production. Yet another study reported decreased secretion of Th1-type cytokines [IFN-γ and tumour necrosis factor (TNF)-α], but enhanced secretion of the Th2 cytokine IL-4, from splenocytes in mice fed a fish oil-enriched diet [18]. The present study

was designed to investigate Ivacaftor cost the hypothesis that intake of long-chain n-3 PUFAs would affect Th1- and Th2-mediated sensitization and/or inflammation differentially. The effects of fish oil (rich in n-3 PUFAs) and sunflower oil (rich in n-6 PUFAs) intake were studied in two mouse hypersensitivity models: Th1-driven delayed-type hypersensitivity (DTH) and Th2-driven IgE production and eosinophil-mediated airway inflammation. In addition, the effect of PUFA consumption on the fatty acid serum profile was evaluated by monitoring serum levels during the study. Four-week-old male BALB/c mice (Scanbur AB, Sollentuna, Sweden) were provided with food and water ad libitum. The mice were fed with one of three diets. The control group received regular

mouse chow containing 1 wt% soya oil (Lantmännen, Lidköping, Sweden). The fish oil group received regular chow supplemented with Carteolol HCl 10 wt% fish oil containing 0·28 g EPA/ml and 0·34 g DHA/ml (Möllers Tran natural; Peter Möller, Oslo, Norway). The sunflower oil group received regular chow supplemented with 10 wt% sunflower oil containing 0·54 g linoleic acid/ml (Coop Solrosolja; Coop Sweden, Solna, Sweden). Permission for the study was granted by the Regional Ethics Committee, University of Gothenburg (no. 408-2008), and the experiments were carried out according to the guidelines of the ‘Council of Europe Convention for the Protection of Vertebrate Animals used for Experimental and Other Scientific purposes’. Th1-mediated hypersensitivity was tested in the DTH model summarized in Fig. 1a. After receiving the experimental or control diet for 21 days, the mice were anaesthetized briefly (Isofluran; Baxter Medical AB, Kista, Sweden) and then each hind leg was injected intramuscularly with 50 µg ovalbumin (OVA) in 50 µl of phosphate-buffered saline (PBS), emulsified in an equal volume of complete Freund’s adjuvant (Difco Laboratories, Detroit, MI, USA).