Abstract:
:The importance of metabolism in macrophage function has been reported, but the in vivo relevance of the in vitro observations is still unclear. Here we show that macrophage metabolites are defined in a specific tissue context, and these metabolites are crucially linked to tissue-resident macrophage functions. We find the peritoneum to be rich in glutamate, a glutaminolysis-fuel that is exploited by peritoneal-resident macrophages to maintain respiratory burst during phagocytosis via enhancing mitochondrial complex-II metabolism. This niche-supported, inducible mitochondrial function is dependent on protein kinase C activity, and is required to fine-tune the cytokine responses that control inflammation. In addition, we find that peritoneal-resident macrophage mitochondria are recruited to phagosomes and produce mitochondrially derived reactive oxygen species, which are necessary for microbial killing. We propose that tissue-resident macrophages are metabolically poised in situ to protect and exploit their tissue-niche by utilising locally available fuels to implement specific metabolic programmes upon microbial sensing.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Davies LC,Rice CM,Palmieri EM,Taylor PR,Kuhns DB,McVicar DWdoi
10.1038/s41467-017-02092-0subject
Has Abstractpub_date
2017-12-12 00:00:00pages
2074issue
1issn
2041-1723pii
10.1038/s41467-017-02092-0journal_volume
8pub_type
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