{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,30]],"date-time":"2026-05-30T00:29:16Z","timestamp":1780100956391,"version":"3.54.0"},"reference-count":41,"publisher":"American Physiological Society","issue":"2","funder":[{"name":"NIH","award":["T32DK007573-23"],"award-info":[{"award-number":["T32DK007573-23"]}]},{"name":"NIH","award":["R01 HL131608"],"award-info":[{"award-number":["R01 HL131608"]}]},{"name":"NIH","award":["HL134828"],"award-info":[{"award-number":["HL134828"]}]},{"name":"NIH","award":["HL126456"],"award-info":[{"award-number":["HL126456"]}]},{"name":"Societe francaise d&apos;Anesthesie-Reanimation"},{"name":"Association Chirurgicale pour le Developpment et l&apos;Amelioration des Techniques de Depistage de Traitment des Maladies Cardiovasculaires"},{"name":"Journees Rennaises d&apos;Anesthesie-Reanimation"},{"name":"CIHR Banting Post-doctoral fellowship"},{"name":"University of Toroto Clinician Scientist Training Program"},{"name":"NIH","award":["R37 HL51856"],"award-info":[{"award-number":["R37 HL51856"]}]},{"name":"NIH","award":["HL134828"],"award-info":[{"award-number":["HL134828"]}]},{"name":"NIH","award":["HL126456"],"award-info":[{"award-number":["HL126456"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[2020,8,1]]},"abstract":"<jats:p> Few patients with bacteremia from a nonpulmonary source develop acute respiratory distress syndrome (ARDS). However, the mechanisms that protect the lung from injury in bacteremia have not been identified. We simulated bacteremia by adding Streptococcus pneumoniae to the perfusate of the ex vivo perfused human lung model. In contrast to a pneumonia model in which bacteria were instilled into the distal air spaces of one lobe, injection of high doses of S. pneumoniae into the perfusate was not associated with alveolar epithelial injury as demonstrated by low protein permeability of the alveolar epithelium, intact alveolar fluid clearance, and the absence of alveolar edema. Unexpectedly, the ex vivo human lung rapidly cleared large quantities of S. pneumoniae even though the perfusate had very few intravascular phagocytes and lacked immunoglobulins or complement. The bacteria were cleared in part by the small number of neutrophils in the perfusate, alveolar macrophages in the airspaces, and probably by interstitial pathways. Together, these findings identify one mechanism by which the lung and the alveolar epithelium are protected from injury in bacteremia. <\/jats:p>","DOI":"10.1152\/ajplung.00053.2020","type":"journal-article","created":{"date-parts":[[2020,6,10]],"date-time":"2020-06-10T12:53:50Z","timestamp":1591793630000},"page":"L218-L227","source":"Crossref","is-referenced-by-count":13,"title":["The ex vivo perfused human lung is resistant to injury by high-dose <i>S. pneumoniae<\/i> bacteremia"],"prefix":"10.1152","volume":"319","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8465-8250","authenticated-orcid":false,"given":"James T.","family":"Ross","sequence":"first","affiliation":[{"name":"Department of Surgery, University of California San Francisco, San Francisco, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicolas","family":"Nesseler","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute, University of California San Francisco, San 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