学术沙龙

学术沙龙第二期:饮食、先天免疫与长寿

发布时间:2020-12-03  阅读次数:2919

报 告 人:吴紫云      农生学院食品科学与工程系     长聘教轨副教授 博导 独立PI

   间:2020年12月9日 (星期三) 12:45-13:30

   点:农生学院创新楼(B楼)104会议室

主办单位:农生学院学科与科技办、农生学院青年教师联谊会

 

 

报告题目:

饮食、先天免疫与长寿

报告摘要:

饮食限制是现代衰老生物学研究一个非常重要的发现,尽管不同的物种寿命相差甚远,但大量的研究表明饮食限制能延长众多真核生物的寿命,比如从非常低等的单细胞生物酿酒酵母到高等的灵长目猕猴等。衰老研究另一个重要的突破就是人们发现一些进化上非常保守的分子信号通路像mTOR或者胰岛素/IGF-1等可以控制不同物种的寿命,即表明衰老是可以控制的。这对于人们开发各种抗衰老方法提供了一个非常重要的理论基础。目前许多研究认为饮食限制或减弱mTOR和胰岛素/IGF-1等营养代谢信号通路能激活下游转录因子,增强细胞的各种抗压等保护机制,从而延长生物的寿命。虽然免疫和炎症对人的衰老有重要影响,但免疫特别是先天免疫如何影响寿命仍不清楚。在该研究中,我们用秀丽线虫(Caenorhabditis elegans)模型发现饮食限制能通过物种间非常保守的p38-ATF-7信号通路来降低天然免疫活性,从而延长线虫寿命。相反,增加饮食可以激活p38-ATF-7天然免疫活性,缩短线虫寿命。有趣的是,该研究发现胰岛素/IGF-1信号通路通过下游转录因子daf-16/FOXO也能调控饮食从而影响p38-ATF-7天然免疫活性和线虫寿命,而mTOR则不调控饮食。因此,该研究为饮食限制与长寿开辟了一个新的分子信号机制,为先天免疫反应和代谢的关系建立了一个新的参考模型,同时饮食激活p38-ATF-7信号通路也暗示饮食可能推动了免疫系统的进化。对人而言,先天免疫和炎症紧密联系,本研究对理解胰岛素/IGF-1-FOXO信号通路如何调控食欲、生长、代谢、炎症以及衰老提供了新的思路。

报告人简介:

【PI学科组研究方向】:

人为什么会衰老?衰老为什么会导致众多衰老相关疾病?以及如何延缓衰老?一直是人类面临的最具挑战性的科学问题。我们课题组长期关注于食品营养与生物衰老相关研究进展,希望从食物营养的角度来寻找长寿的秘诀,为国家“健康中国2030”规划和老年人的健康做出贡献。当前课题组重点研究领域:1、长寿膳食配方的研究;2、营养代谢调控衰老的分子机制;3、先天免疫影响衰老的分子机制。

【报告人代表性著作】:

1.Wu Z, Isik M, Moroz N, Steinbaugh MJ, Zhang P and Blackwell TK. Dietary restriction extends lifespan through metabolic regulation of innate immunity. Cell Metabolism, 2019, 29(5), 1192-1205.

2.Wu Z, Senchuk MM, Dues DJ, Johnson BK, Cooper JF, Lew L, Machiela E, Schaar CE, DeJonge H, Blackwell TK and Van Raamsdonk JM. Mitochondrial unfolded protein response transcription factor ATFS-1 promotes longevity in a long-lived mitochondrial mutant through activation of stress response pathways. BMC Biology, 2018, 16, 147.

 

 

ACADEMIC SALON (II )

SPEAKER: Ziyun Wu

Tenure-track Associate Professor, Ph.D. Supervisor, PI

Department of Food Science & Engineering, SAB

TIME:12:45-13:30  Dec 9, 2020  (Wed)

VENUE:Room 104, Building B, SAB

ORGANIZER:Office of Discipline and Science & Technology, SAB;

Young Teachers Association, SAB

TITLE:Food intake, innate immunity and longevity

ABSTRACT:

An important hallmark of human aging is immune dysregulation.  Aging increases chronic innate immune activity and inflammation, a major risk factor for age-related pathologies that include diabetes, cancer, and neurodegenerative and cardiovascular disease. The emerging idea that innate immunity is influenced by metabolic activity is of great interest, because of the potential importance in metabolic disease, but it is unknown whether immunity regulation might be important for extending healthy lifespan.  Here we show that in C. elegans, dietary restriction (DR) extends lifespan by modulating a conserved innate immunity pathway that is regulated by p38 signaling, and the transcription factor ATF-7.  Longevity from DR depends upon p38–ATF-7 immunity being intact, but downregulated to a basal level.  p38–ATF-7 immunity accelerates aging when hyperactive, influences lifespan independently of pathogen exposure, and is activated by nutrients independently of mTORC1, a major DR mediator.  Longevity from reduced insulin/IGF-1 signaling (rIIS) also involves p38–ATF-7 downregulation, with signals from DAF-16/FOXO reducing food intake.  We conclude that p38–ATF-7 is an immunometabolic pathway that senses bacterial and nutrient signals, that immunity modulation is critical for DR, and that DAF-16/FOXO couples appetite to growth regulation.  These conserved mechanisms may influence aging in more complex organisms. An understanding of how the p38–ATF-7 pathway is regulated by nutrients and bacterial signals, and feeding by DAF-16, may therefore reveal new possibilities for influencing human appetite, immunity, and longevity.

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