{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Palmer CD"],"funding":["Greene Fund","Dana Human Immunology Award","Thrasher Foundation","Defense Advanced Projects Agency","NIAID NIH HHS","American Recovery and Reinvestmant Act NIH Administrative Supplement","NHLBI NIH HHS","DARPA","NIH","Dartmouth Center for Medical Countermeasures Pilot Project","NIGMS NIH HHS"],"pagination":["459-70"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3157902"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["90(3)"],"pubmed_abstract":["Detection and clearance of bacterial infection require balanced effector and resolution signals to avoid chronic inflammation. Detection of GNB LPS by TLR4 on m induces inflammatory responses, contributing to chronic inflammation and tissue injury. LXs and Rvs are endogenous lipid mediators that enhance resolution of inflammation, and their actions on primary human m responses toward GNB are largely uncharacterized. Here, we report that LXA(4), LXB(4), and RvD1, tested at 0.1-1 μM, inhibited LPS-induced TNF production from primary human m, with ATL and 17(R)-RvD1, demonstrating potent inhibition at 0.1 μM. In addition, 17(R)-RvD1 inhibited LPS-induced primary human m production of IL-7, IL-12p70, GM-CSF, IL-8, CCL2, and MIP-1α without reducing that of IL-6 or IL-10. Remarkably, when stimul"],"journal":["Journal of leukocyte biology"],"pubmed_title":["17(R)-Resolvin D1 differentially regulates TLR4-mediated responses of primary human macrophages to purified LPS and live E. coli."],"pmcid":["PMC3157902"],"funding_grant_id":["R21 HL089659-01A1","RO1 AI067353","R01 AI067353","P01 GM095467","R21 HL089659","3R01AI067353-05S1","R01 GM038765","R01GM038765","P01GM095467"],"pubmed_authors":["Mancuso CJ","Serhan CN","Weiss JP","Palmer CD","Levy O","Guinan EC"],"additional_accession":[]},"is_claimable":false,"name":"17(R)-Resolvin D1 differentially regulates TLR4-mediated responses of primary human macrophages to purified LPS and live E. coli.","description":"Detection and clearance of bacterial infection require balanced effector and resolution signals to avoid chronic inflammation. Detection of GNB LPS by TLR4 on m induces inflammatory responses, contributing to chronic inflammation and tissue injury. LXs and Rvs are endogenous lipid mediators that enhance resolution of inflammation, and their actions on primary human m responses toward GNB are largely uncharacterized. Here, we report that LXA(4), LXB(4), and RvD1, tested at 0.1-1 μM, inhibited LPS-induced TNF production from primary human m, with ATL and 17(R)-RvD1, demonstrating potent inhibition at 0.1 μM. In addition, 17(R)-RvD1 inhibited LPS-induced primary human m production of IL-7, IL-12p70, GM-CSF, IL-8, CCL2, and MIP-1α without reducing that of IL-6 or IL-10. Remarkably, when stimul","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Sep","modification":"2025-07-11T03:04:01.108Z","creation":"2025-07-11T03:04:01.108Z"},"accession":"S-EPMC3157902","cross_references":{"pubmed":["21653234"],"doi":["10.1189/jlb.0311145"]}}