Growth performance and immune responses in chickens after challenge with lipopolysaccharide and modulation by dietary different oils
- PMID: 22445015
- DOI: 10.1017/S1751731107001188
Growth performance and immune responses in chickens after challenge with lipopolysaccharide and modulation by dietary different oils
Abstract
The study was conducted to investigate the effects of different oils on growth performance and immune responses of chickens after challenge with lipopolysaccharide (LPS). A total of 288 chickens were assigned in a 2 × 2 factorial design. Factors were dietary fat type (4.5% maize oil or 4.5% fish oil) and immunological challenge (LPS or saline). At 20 days and 27 days of age, chickens were injected intraperitoneally with either 1 mg/kg body weight of LPS or sterile saline. LPS decreased feed intake from 21 days to 28 days of age and body-weight gain from 21 days to 42 days of age. Fish oil improved feed-conversion efficiency of chickens after LPS challenge for the first time. Fish oil supplementation decreased lymphocyte proliferation (21 days: P < 0.0001; 28 days: P < 0.0001) and the ratio of CD3+CD4+/CD3+CD8+ (21 days: P = 0.0479; 28 days: P = 0.0009) after LPS challenge. LPS challenge increased the levels of interleukin-1 (IL-1) (21 days: P < 0.0001; 28 days: P = 0.0030), IL-6 (21 days: P < 0.0001; 28 days: P = 0.0001) and tumor necrosis factor-α (TNF-α) (21 days: P = 0.0008; 28 days: P = 0.0018). And fish oil alleviated the elevations in the production of IL-6 (21 days: P = 0.0359; 28 days: P = 0.0302) and TNF-α (21 days: P = 0.0055; 28 days: P = 0.0391) induced by the LPS challenge. Fish oil alleviated the mRNA abundance elevation of nuclear factor kappa B (NFκB) (21 days: P = 0.0079; 28 days: P = 0.0017) after LPS challenge. These results showed that fish oil acts as an anti-inflammatory agent, which may be associated with down-regulation of the activated immune system. The results of pro-inflammatory cytokines and mRNA abundance results suggested that fish oil might alleviate the elevation of IL-6 and TNF-α induced by LPS through down-regulating NFκB expression.
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