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돼지에서 분리된 Lactobacillus strains의 균체분해산물에 의한 RAW 264.7 Macrophage 활성화

Activation of RAW 264.7 Macrophage by Digested Bacterial Cell of Pig-derived Lactobacillus Strains

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참고문헌

주제분류축산학

초록

경구로 섭취된 생균제가 소화관 효소의 작용을 받은 경우 장관면역계의 macrophage에 미치는 영향을 조사하기 위하여 돼지의 장내에서 분리된 lactobacilli를 pepsin과 pancreatin과 같은 소화관 효소로 분해한 균체분해산물에 의해 RAW 264.7 murine macrophage에서 유도되는 NO, TNF-α 및 IL-6의 생성을 측정하였다. Macrophage에서 유도되는 NO, TNF-α 및 IL-6는 균종과 균체분해산물의 양에 따라 달랐다. NO의 생성수준은 10~150 ug/ml의 분해물에서 관찰 되었으나 TNF-α와 IL-6는 50~300 ug/ml의 고농도처리에서 나타났다. 6개의 Lactobacillus strains 중에서 3149와 3156 균주는 다른 균주에 비해 TNF-α와 IL-6 유도능이 높았다. 또한 소화관 효소에 의해 분해된 lactobacilli의 균체분해산물의 성분이 macrophage 활성 증가와 관련이 있으며 생체내에서 숙주면역계를 조절할 것으로 사료된다. 본 시험에서 사용한 방법은 소화관 면역계에 미치는 유산균의 효과를 규명하는데 유익할 것이다.

Abstract

This study was conducted to investigate the effects of hydrolyzed Lactobacillus supplementation with digestive enzymes treatment on the macrophage activation, the induction of nitric oxide(NO), interleukin (IL)-6 and tumor necrosis factor(TNF)-α. The RAW 264.7 murine macrophage was exposed to porcine Lactobacillus strains which were digested with both pepsin and pancreatin. The production of NO, TNF-α and IL-6 in the macrophage were strain and dose-dependent, respectively. The induction of NO and cytokines were higher in both 3149 and 3146 strains compared with other Lactobacillus strains. Overall, the level of NO was observed at the lower range between 10 and 150 μg hydrolysates per ml, whereas IL-6 and TNF-α were observed at relatively higher concentration between 50 and 300 μg hydrolysates per ml. Lactobacillus strains which produced a high level of NO also showed a high induction of TNF-α and IL-6. Therefore, the present results suggest that hydrolysates of Lactobacillus strains are related to induction of several macrophage mediators, and then it could be beneficially used to modulate gastrointestinal immune function of the host. Also, the methodogly employed in this study might be useful to investigate the effects of lactic acid bacteria on gastrointestinal immunity.

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