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Effect of omega-3 fatty acid supplementation on resolvin (RvE1)-mediated suppression of inflammation in a mouse model of asthma.
Immunopharmacology and Immunotoxicology 2019 March 9
OBJECTIVE: ResolvinE1 (RvE1), an endogenous lipid mediator derived from omega 3 fatty acids contributes to resolution of allergic inflammatory responses. We investigated effects of RvE1 (R) and omega 3 fatty acids (O) on airway reactivity and inflammation using allergic mice.
METHODS: Mice were divided into control (nonasthmatic; CON) and allergen sensitized-challenged (asthmatic; SEN) groups, and were sensitized i.p. on days 1, 6 with 0.2 μg ovalbumin (OVA) followed by 5% OVA aerosol challenges on days 11-13. RvE1 was administered i.p. postallergen challenge, while omega 3 fatty acids (fish oil) were administered via oral gavage once daily (days 1-13). Whole body plethysmography and bronchoalveolar lavage (BAL) studies were performed on day 14.
RESULTS: RvE1 attenuated airway responsiveness to methacholine (48 mg/ml) in treated asthmatic mice vs. nontreated (150 ± 27.88% in SEN vs. 54 ± 7.52% in SEN + R, p < .05). No difference was observed with omega-3 supplementation (115 ± 19.28% in SEN + O) or treatment with both RvE1 and omega 3 fatty acids (39 ± 12.37% in SEN + R + O vs. 54 ± 7.52% in SEN + R). Differential BAL cell analysis showed that RvE1 decreased eosinophils and neutrophils in SEN mice (p < .005) while no difference was observed with omega-3 fatty acids. SEN + R + O group had similar results as RvE1 treated mice, suggesting that only RvE1 attenuated inflammation.
CONCLUSIONS: RvE1 attenuated airway responsiveness and inflammation in asthmatic mice. Omega-3 fatty acids, although a precursor for RvE1 formation, had no additive effects on RvE1 decreases in airway inflammation and airway reactivity. Our data suggests that omega-3 supplementation has little effect on airway inflammation and reactivity in our model of asthma.
METHODS: Mice were divided into control (nonasthmatic; CON) and allergen sensitized-challenged (asthmatic; SEN) groups, and were sensitized i.p. on days 1, 6 with 0.2 μg ovalbumin (OVA) followed by 5% OVA aerosol challenges on days 11-13. RvE1 was administered i.p. postallergen challenge, while omega 3 fatty acids (fish oil) were administered via oral gavage once daily (days 1-13). Whole body plethysmography and bronchoalveolar lavage (BAL) studies were performed on day 14.
RESULTS: RvE1 attenuated airway responsiveness to methacholine (48 mg/ml) in treated asthmatic mice vs. nontreated (150 ± 27.88% in SEN vs. 54 ± 7.52% in SEN + R, p < .05). No difference was observed with omega-3 supplementation (115 ± 19.28% in SEN + O) or treatment with both RvE1 and omega 3 fatty acids (39 ± 12.37% in SEN + R + O vs. 54 ± 7.52% in SEN + R). Differential BAL cell analysis showed that RvE1 decreased eosinophils and neutrophils in SEN mice (p < .005) while no difference was observed with omega-3 fatty acids. SEN + R + O group had similar results as RvE1 treated mice, suggesting that only RvE1 attenuated inflammation.
CONCLUSIONS: RvE1 attenuated airway responsiveness and inflammation in asthmatic mice. Omega-3 fatty acids, although a precursor for RvE1 formation, had no additive effects on RvE1 decreases in airway inflammation and airway reactivity. Our data suggests that omega-3 supplementation has little effect on airway inflammation and reactivity in our model of asthma.
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