Journal
INFECTION AND IMMUNITY
Volume 88, Issue 8, Pages -Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.00130-20
Keywords
Caenorhabditis elegans; Cryptococcus neoformans; Enterococcus faecalis; Pseudomonas aeruginosa; fatty acids; immune response; metabolism; nuclear hormone receptor; nutritional immunity
Categories
Funding
- NIH Office of Infrastructure Programs [P40 OD01440]
- University Grants Commission of the Government of India
- Wellcome Trust/DBT India Alliance Intermediate Fellowship [IA/I/13/1/500919]
- DST-FIST [SR/FST/LS11-036/2014(C)]
- UGC-SAP [F.4.13/2018/DRS-III (SAP-II)]
- DBT-IISc Partnership Program Phase-II [BT/PR27952-INF/22/212/2018]
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Immune response to pathogens is energetically expensive to the host; however, the cellular source of energy to fuel immune response remains unknown. In this study, we show that Caenorhabditis elegans exposed to pathogenic Gram-positive and Gram-negative bacteria or yeast rapidly utilizes lipid droplets, the major energy reserve. The nematode's response to the pathogenic bacterium Enterococcus faecalis entails metabolic rewiring for the upregulation of several genes involved in lipid utilization and downregulation of lipid synthesis genes. Genes encoding acyl-CoA synthetase ACS-2, involved in lipid metabolism, and flavin monooxygenase FMO-2, involved in detoxification, are two highly upregulated genes during E. faecalis infection. We find that both ACS-2 and FMO-2 are necessary for survival and rely on NHR-49, a peroxisome proliferator-activated receptor alpha (PPAR alpha) ortholog, for upregulation during E. faecalis infection. Thus, NHR-49 regulates an immunometabolic axis of survival in C. elegans by modulating breakdown of lipids as well as immune effector production upon E. faecalis exposure.
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