{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T00:08:39Z","timestamp":1792714119532,"version":"4.5.0"},"reference-count":50,"publisher":"American Society for Clinical Investigation","issue":"18","license":[{"start":{"date-parts":[[2022,11,20]],"date-time":"2022-11-20T00:00:00Z","timestamp":1668902400000},"content-version":"vor","delay-in-days":59,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Academia Sinica","award":["107-2101-01-18-03,AS-IA-109-L02,AS-TM-108-02-10,AS-BRPT-110-02"],"award-info":[{"award-number":["107-2101-01-18-03,AS-IA-109-L02,AS-TM-108-02-10,AS-BRPT-110-02"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,9,22]]},"abstract":"<jats:p>\n                    <jats:italic>Pseudomonas aeruginosa<\/jats:italic>\n                    is one of the most common nosocomial infections worldwide, and it frequently causes ventilator-associated acute pneumonia in immunocompromised patients. Abundant neutrophil extracellular traps (NETs) contribute to acute lung injury, thereby aggravating ventilator-induced lung damage. While pattern recognition receptors (PRRs) TLR4 and TLR5 are required for host defense against\n                    <jats:italic>P<\/jats:italic>\n                    .\n                    <jats:italic>aeruginosa<\/jats:italic>\n                    invasion, the PRR responsible for\n                    <jats:italic>P<\/jats:italic>\n                    .\n                    <jats:italic>aeruginosa<\/jats:italic>\n                    \u2013induced NET formation, proinflammatory cytokine release, and acute lung injury remains unclear. We found that myeloid C-type lectin domain family 5 member A (CLEC5A) interacts with LPS of\n                    <jats:italic>P<\/jats:italic>\n                    .\n                    <jats:italic>aeruginosa<\/jats:italic>\n                    and is responsible for\n                    <jats:italic>P<\/jats:italic>\n                    .\n                    <jats:italic>aeruginosa<\/jats:italic>\n                    \u2013induced NET formation and lung inflammation.\n                    <jats:italic>P<\/jats:italic>\n                    .\n                    <jats:italic>aeruginosa<\/jats:italic>\n                    activates CLEC5A to induce caspase-1\u2013dependent NET formation, but it neither causes gasdermin D (GSDMD) cleavage nor contributes to\n                    <jats:italic>P<\/jats:italic>\n                    .\n                    <jats:italic>aeruginosa<\/jats:italic>\n                    \u2013induced neutrophil death. Blockade of CLEC5A attenuates\n                    <jats:italic>P<\/jats:italic>\n                    .\n                    <jats:italic>aeruginosa<\/jats:italic>\n                    \u2013induced NETosis and lung injury, and simultaneous administration of anti-CLEC5A mAb with ciprofloxacin increases survival rate and decreases collagen deposition in the lungs of mice challenged with a lethal dose of\n                    <jats:italic>P<\/jats:italic>\n                    .\n                    <jats:italic>aeruginosa<\/jats:italic>\n                    . Thus, CLEC5A is a promising therapeutic target to reduce ventilator-associated lung injury and fibrosis in\n                    <jats:italic>P<\/jats:italic>\n                    .\n                    <jats:italic>aeruginosa<\/jats:italic>\n                    \u2013induced pneumonia.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.156613","type":"journal-article","created":{"date-parts":[[2022,9,1]],"date-time":"2022-09-01T12:00:56Z","timestamp":1662033656000},"source":"Crossref","is-referenced-by-count":53,"title":["CLEC5A is critical in Pseudomonas aeruginosa\u2013induced NET formation and acute lung injury"],"prefix":"10.1172","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5061-4989","authenticated-orcid":true,"given":"Pei-Shan","family":"Sung","sequence":"first","affiliation":[{"name":"Genomics Research Center, Academia Sinica, Taipei, 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