{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Earhart AP"],"funding":["NHLBI NIH HHS","NCI NIH HHS"],"pubmed_abstract":["Complement protein C3 is crucial for immune responses in mucosal sites such as the lung, where it aids in microbe elimination and enhances inflammation. While trained immunity - enhanced secondary responses of innate immune cells after prior exposure - is well-studied, the role of the complement system in trained immune responses remains unclear. We investigated the role of C3 in trained immunity and found that <i>in vivo</i>, trained wild-type mice showed significantly elevated pro-inflammatory cytokines and increased C3a levels upon a second stimulus, whereas C3-deficient mice exhibited a blunted cytokine response and heightened evidence of lung injury. <i>Ex vivo</i>, C3-deficient alveolar macrophages (AMs) displayed reduced chemokine and cytokine output after training, which was restor"],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2024.11.01.621042"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11565986"],"repository":["biostudies-literature"],"pubmed_title":["The C3-C3aR axis modulates trained immunity in alveolar macrophages."],"pmcid":["PMC11565986"],"funding_grant_id":["P30 CA091842","T32 HL125241","R01 HL169860"],"pubmed_authors":["Garnica L","Kulkarni HS","Earhart AP","Nallapu A","Haspel JA","Ozanturk AN","Alburquerque RA","Maurya RK","Starick M","Wu X"],"additional_accession":[]},"is_claimable":false,"name":"The C3-C3aR axis modulates trained immunity in alveolar macrophages.","description":"Complement protein C3 is crucial for immune responses in mucosal sites such as the lung, where it aids in microbe elimination and enhances inflammation. While trained immunity - enhanced secondary responses of innate immune cells after prior exposure - is well-studied, the role of the complement system in trained immune responses remains unclear. We investigated the role of C3 in trained immunity and found that <i>in vivo</i>, trained wild-type mice showed significantly elevated pro-inflammatory cytokines and increased C3a levels upon a second stimulus, whereas C3-deficient mice exhibited a blunted cytokine response and heightened evidence of lung injury. <i>Ex vivo</i>, C3-deficient alveolar macrophages (AMs) displayed reduced chemokine and cytokine output after training, which was restor","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2025-04-04T02:12:24.606Z","creation":"2025-04-04T02:12:24.606Z"},"accession":"S-EPMC11565986","cross_references":{"pubmed":["39554000"],"doi":["10.1101/2024.11.01.621042"]}}