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dc.contributor.authorKorkmaz, Filiz T
dc.contributor.authorShenoy, Anukul T
dc.contributor.authorSymer, Elise M
dc.contributor.authorBaird, Lillia A
dc.contributor.authorOdom, Christine V
dc.contributor.authorArafa, Emad I
dc.contributor.authorDimbo, Ernest L
dc.contributor.authorNa, Elim
dc.contributor.authorMolina-Arocho, William
dc.contributor.authorBrudner, Matthew
dc.contributor.authorStandiford, Theodore J
dc.contributor.authorMehta, Jawahar L
dc.contributor.authorSawamura, Tatsuya
dc.contributor.authorJones, Matthew R
dc.contributor.authorMizgerd, Joseph P
dc.contributor.authorTraber, Katrina E
dc.contributor.authorQuinton, Lee J
dc.date.accessioned2024-04-26T19:51:21Z
dc.date.available2024-04-26T19:51:21Z
dc.date.issued2022-12-08
dc.identifier.citationKorkmaz FT, Shenoy AT, Symer EM, Baird LA, Odom CV, Arafa EI, Dimbo EL, Na E, Molina-Arocho W, Brudner M, Standiford TJ, Mehta JL, Sawamura T, Jones MR, Mizgerd JP, Traber KE, Quinton LJ. Lectin-like oxidized low-density lipoprotein receptor 1 attenuates pneumonia-induced lung injury. JCI Insight. 2022 Dec 8;7(23):e149955. doi: 10.1172/jci.insight.149955. PMID: 36264633; PMCID: PMC9746901.en_US
dc.identifier.eissn2379-3708
dc.identifier.doi10.1172/jci.insight.149955en_US
dc.identifier.pmid36264633
dc.identifier.urihttp://hdl.handle.net/20.500.14038/53306
dc.description.abstractIdentifying host factors that contribute to pneumonia incidence and severity are of utmost importance to guiding the development of more effective therapies. Lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1, encoded by OLR1) is a scavenger receptor known to promote vascular injury and inflammation, but whether and how LOX-1 functions in the lung are unknown. Here, we provide evidence of substantial accumulation of LOX-1 in the lungs of patients with acute respiratory distress syndrome and in mice with pneumonia. Unlike previously described injurious contributions of LOX-1, we found that LOX-1 is uniquely protective in the pulmonary airspaces, limiting proteinaceous edema and inflammation. We also identified alveolar macrophages and recruited neutrophils as 2 prominent sites of LOX-1 expression in the lungs, whereby macrophages are capable of further induction during pneumonia and neutrophils exhibit a rapid, but heterogenous, elevation of LOX-1 in the infected lung. Blockade of LOX-1 led to dysregulated immune signaling in alveolar macrophages, marked by alterations in activation markers and a concomitant elevation of inflammatory gene networks. However, bone marrow chimeras also suggested a prominent role for neutrophils in LOX-1-mediated lung protection, further supported by LOX-1+ neutrophils exhibiting transcriptional changes consistent with reparative processes. Taken together, this work establishes LOX-1 as a tissue-protective factor in the lungs during pneumonia, possibly mediated by its influence on immune signaling in alveolar macrophages and LOX-1+ airspace neutrophils.en_US
dc.language.isoenen_US
dc.relation.ispartofJCI Insighten_US
dc.relation.urlhttps://doi.org/10.1172/jci.insight.149955en_US
dc.rightsCopyright: © 2022, Korkmaz et al. This is an open access article published under the terms of the Creative Commons Attribution 4.0 International License.en_US
dc.rightsAttribution 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectBacterial infectionsen_US
dc.subjectCellular immune responseen_US
dc.subjectImmunologyen_US
dc.subjectInflammationen_US
dc.subjectInnate immunityen_US
dc.titleLectin-like oxidized low-density lipoprotein receptor 1 attenuates pneumonia-induced lung injuryen_US
dc.typeJournal Articleen_US
dc.source.journaltitleJCI insight
dc.source.volume7
dc.source.issue23
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.identifier.journalJCI insight
refterms.dateFOA2024-04-26T19:51:23Z
dc.contributor.departmentMedicineen_US


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Copyright: © 2022, Korkmaz et
al. This is an open access article
published under the terms of the
Creative Commons Attribution 4.0
International License.
Except where otherwise noted, this item's license is described as Copyright: © 2022, Korkmaz et al. This is an open access article published under the terms of the Creative Commons Attribution 4.0 International License.