Mechanism underlying prolongevity induced by bifidobacteria in Caenorhabditis elegans
Mechanism underlying prolongevity induced by bifidobacteria in Caenorhabditis elegans
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DOI：
10.1007/s10522-012-9411-6
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发表时间：
2013-02-01
期刊：
影响因子：
4.5
通讯作者：
Nishikawa, Yoshikazu
中科院分区：
文献类型：
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作者：
Komura, Tomomi;Ikeda, Takanori;Nishikawa, Yoshikazu
乳酸杆菌和双歧杆菌是益生菌，其改变宿主防御系统并且具有延长线虫秀丽隐杆线虫的寿命的能力。在此，我们试图阐明双歧杆菌延长C.优雅的。以双歧杆菌（Bifidobacteriums，BI）与标准食用菌大肠杆菌（Escherichiacoli）OP 50（OP 50）按不同比例混合饲喂线虫，蠕虫的平均寿命呈剂量依赖性延长。饲喂BI的蠕虫比对照蠕虫表现出更高的运动能力和产生更多的后代。无论BI与OP的混合量如何，线虫的生长曲线都是相似的，这表明BI不会通过热量限制诱导存活效应。值得注意的是，仅用BI的细胞壁部分喂养蠕虫足以促进存活。蛋白质羰基和脂褐素，老化的生化标志物的积累，也较低的蠕虫喂养BI，然而，蠕虫显示类似的敏感性热，过氧化氢，百草枯，自由基的诱导剂，作为控制蠕虫。作为BI喂养的结果，daf-16、jnk-1、aak-2、tol-1和tir-1的功能丧失突变体表现出比OP喂养的对照蠕虫更长的寿命，但BI未能延长pad 3 -1、skn-1和vhp-1突变体的寿命。由于skn-1诱导2期解毒酶，我们的研究结果表明，双歧杆菌的细胞壁成分增加了C。通过激活skn-1，由p38 MAPK途径调节，但不是通过激活宿主防御系统，通过p38 MAPK-16。
Lactobacilli and bifidobacteria are probiotic bacteria that modify host defense systems and have the ability to extend the lifespan of the nematode Caenorhabditis elegans. Here, we attempted to elucidate the mechanism by which bifidobacteria prolong the lifespan of C. elegans. When the nematode was fed Bifidobacterium infantis (BI) mixed at various ratios with the standard food bacterium Escherichia coli strain OP50 (OP), the mean lifespan of worms was extended in a dose-dependent manner. Worms fed BI displayed higher locomotion and produced more offspring than control worms. The growth curves of nematodes were similar regardless of the amount of BI mixed with OP, suggesting that BI did not induce prolongevity effects through caloric restriction. Notably, feeding worms the cell wall fraction of BI alone was sufficient to promote prolongevity. The accumulation of protein carbonyls and lipofuscin, a biochemical marker of aging, was also lower in worms fed BI; however, the worms displayed similar susceptibility to heat, hydrogen peroxide, and paraquat, an inducer of free radicals, as the control worms. As a result of BI feeding, loss-of-function mutants of daf-16, jnk-1, aak-2, tol-1, and tir-1 exhibited a longer lifespan than OP-fed control worms, but BI failed to extend the lifespan of pmk-1, skn-1, and vhp-1 mutants. As skn-1 induces phase 2 detoxification enzymes, our findings suggest that cell wall components of bifidobacteria increase the average lifespan of C. elegans via activation of skn-1, regulated by the p38 MAPK pathway, but not by general activation of the host defense system via DAF-16.