{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T23:18:57Z","timestamp":1791847137185,"version":"4.3.4"},"reference-count":41,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2011,11,1]],"date-time":"2011-11-01T00:00:00Z","timestamp":1320105600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2011,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Lung macrophages use the scavenger receptor MARCO to bind and ingest bacteria, particulate matter, and post cellular debris. We investigated the role of MARCO in influenza A virus (IAV) pneumonia. In contrast to higher susceptibility to bacterial infection, MARCO\u2212\/\u2212 mice had lower morbidity and mortality from influenza pneumonia than wild-type (WT) mice. The early course of influenza in MARCO\u2212\/\u2212 lungs was marked by an enhanced but transient neutrophilic inflammatory response and significantly lower viral replication compared with the WT mice. At later time points, no significant differences in lung histopathology or absolute numbers of T lymphocyte influx were evident. Uptake of IAV by WT and MARCO\u2212\/\u2212 bronchoalveolar lavage macrophages in vitro was similar. By LPS coadministration, we demonstrated that rapid neutrophil and monocyte influx during the onset of influenza suppressed viral replication, indicating a protective role of early inflammation. We hypothesized that the presence of increased basal proinflammatory post cellular debris in the absence of scavenging function lowered the inflammatory response threshold to IAV in MARCO\u2212\/\u2212 mice. Indeed, MARCO\u2212\/\u2212 mice showed increased accumulation of proinflammatory oxidized lipoproteins in the bronchoalveolar lavage early in the infection process, which are the potential mediators of the observed enhanced inflammation. These results indicate that MARCO suppresses a protective early inflammatory response to influenza, which modulates viral clearance and delays recovery.<\/jats:p>","DOI":"10.1165\/rcmb.2010-0349oc","type":"journal-article","created":{"date-parts":[[2011,5,12]],"date-time":"2011-05-12T01:46:20Z","timestamp":1305164780000},"page":"1036-1044","source":"Crossref","is-referenced-by-count":65,"title":["MARCO Regulates Early Inflammatory Responses against Influenza"],"prefix":"10.1093","volume":"45","author":[{"given":"Sanjukta","family":"Ghosh","sequence":"first","affiliation":[{"name":"Department of Integrative and Molecular Physiological Sciences, Harvard School of Public Health, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Gregory","sequence":"additional","affiliation":[{"name":"Department of Integrative and Molecular Physiological Sciences, Harvard School of Public Health, Boston, 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