{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T19:39:42Z","timestamp":1787168382575,"version":"build-2736575974"},"reference-count":73,"publisher":"Rockefeller University Press","issue":"4","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2013,4,8]]},"abstract":"<jats:p>The bone marrow\u2013derived cell (BMDC)\u2013associated inflammatory response plays a key role in the development of acute lung injury (ALI). Activation of adenosine A2A receptor (A2AR) is generally considered to be antiinflammatory, inhibiting BMDC activities to protect against ALI. However, in the present study, we found that in a mouse model of neurogenic ALI induced by severe traumatic brain injury (TBI), BMDC A2AR exerted a proinflammatory effect, aggravating lung damage. This is in contrast to the antiinflammatory effect observed in the mouse oleic acid\u2013induced ALI model (a nonneurogenic ALI model.) Moreover, the A2AR agonist CGS21680 aggravated, whereas the antagonist ZM241385 attenuated, the severe TBI-induced lung inflammatory damage in mice. Further investigation of white blood cells isolated from patients or mouse TBI models and of cultured human or mouse neutrophils demonstrated that elevated plasma glutamate after severe TBI induced interaction between A2AR and the metabotropic glutamate receptor 5 (mGluR5) to increase phospholipase C\u2013protein kinase C signaling, which mediated the proinflammatory effect of A2AR. These results are in striking contrast to the well-known antiinflammatory and protective role of A2AR in nonneurogenic ALI and indicate different therapeutic strategies should be used for nonneurogenic and neurogenic ALI treatment when targeting A2AR.<\/jats:p>","DOI":"10.1084\/jem.20122196","type":"journal-article","created":{"date-parts":[[2013,3,12]],"date-time":"2013-03-12T00:02:03Z","timestamp":1363046523000},"page":"839-851","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":43,"title":["Plasma glutamate\u2013modulated interaction of A2AR and mGluR5 on BMDCs aggravates traumatic brain injury\u2013induced acute lung injury"],"prefix":"10.1084","volume":"210","author":[{"given":"Shuang-Shuang","family":"Dai","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology 1 and 2 and 3"},{"name":"Molecular Biology Center, State Key Laboratory of Trauma, Burn, and Combined Injury 1 and 2 and 3"},{"name":"Department of Neurosurgery, Research Institute of Surgery and Daping Hospital; 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