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Temperature perception by ER UPR promotes preventive innate immunity and longevity
Lei Zhou1, Haoyu Zhuo1, Jiaqi Jin1
1State Key Laboratory of Resource Insects, Key Laboratory for Sericulture Biology and Genetic Breeding, Ministry of Agriculture and Rural Affairs, College of Sericulture, Textile and Biomass Sciences, Southwest University, Chongqing 400715, China.
Cell Reports
|December 15, 2024
Summary
Rising environmental temperatures boost innate immunity via endoplasmic reticulum unfolded protein response (ER-UPR), distinct from pathogen responses. This temperature-sensing mechanism impacts lipid accumulation, immune pathways, and lifespan regulation.
Area of Science:
- Immunology
- Environmental Health
- Cellular Biology
Background:
- Microbial infections increase with rising environmental temperatures, posing risks to hosts.
- Host basal immunity activates to counter threats, but sensing temperature changes to adjust immunity is unclear.
Purpose of the Study:
- Investigate how animals sense temperature elevation to modulate preventive immune responses.
- Elucidate the distinct mechanisms of temperature-induced versus pathogen-induced immunity.
Main Methods:
- Utilized a model organism to study temperature-induced immune activation.
- Investigated the role of the endoplasmic reticulum (ER) unfolded protein response (UPR) pathway.
- Analyzed the impact of XBP-1 UPR activation on ribosome biogenesis and lipid metabolism.
Main Results:
- High temperature activates the ER-UPR, unlike pathogen invasion which requires mitochondrial UPR.
- Chronic ER-UPR activation represses ribosome biogenesis, causing lipid accumulation.
- Increased oleic acid from lipid accumulation activates the PMK-1 immune pathway.
- Ribosome biogenesis regulates longevity, influenced by lipid metabolism and innate immunity.
Conclusions:
- Endoplasmic reticulum-nucleolus crosstalk is vital for preventive immunity and lifespan regulation.
- Temperature sensing by the ER-UPR is a key mechanism for innate immune adjustment.
- Findings reveal novel links between cellular stress responses, metabolism, immunity, and aging.
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