{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T13:35:40Z","timestamp":1789565740721,"version":"build-2803163510"},"reference-count":38,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2017,2,1]],"date-time":"2017-02-01T00:00:00Z","timestamp":1485907200000},"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":[[2017,2,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Neutrophils are considered responsible for the pathophysiological changes resulting from hepatic ischemia-reperfusion (I\/R) injury, which is a complication of trauma, shock, liver resection, and transplantation. Recently, evidence is accumulating that formyl-peptide receptor (FPR) signaling constitutes an important danger signal that guides neutrophils to sites of inflammation. This study aimed to investigate dynamic neutrophil recruitment using two-photon laser-scanning microscopy (TPLSM) in response to FPR1 blockade during hepatic I\/R. LysM-eGFP mice were subjected to partial warm hepatic I\/R. They were pretreated with an FPR1 antagonist, cyclosporine H (CsH), or formyl peptide, fMLF. Liver was imaged after hepatic laser irradiation or I\/R using the TPLSM technique. CsH treatment alleviated hepatic I\/R injury, as evidenced by decreased serum transaminase levels, reduced hepatocyte necrosis\/apoptosis, and diminished inflammatory cytokine, chemokine, and oxidative stress. In contrast, systemic administration of fMLF showed few effects. Time-lapse TPLSM showed that FPR1 blockade inhibited the accumulation of neutrophils in the necrotic area induced by laser irradiation in vivo. In the CsH-treated I\/R group, the number and crawling velocity of neutrophils in the nonperfused area were lower than those in the control group. Meanwhile, FPR1 blockade did not affect monocyte\/macrophage recruitment. Hepatic I\/R promoted the retention of neutrophils and their active behavior in the spleen, whereas CsH treatment prevented their changes. Intravital TPLSM revealed that formyl-peptide\u2013FPR1 signaling is responsible for regulating neutrophil chemotaxis to allow migration into the necrotic area in hepatic I\/R. Our findings suggest effective approaches for elucidating the mechanisms of immune cell responses in hepatic I\/R.<\/jats:p>","DOI":"10.4049\/jimmunol.1601773","type":"journal-article","created":{"date-parts":[[2017,1,7]],"date-time":"2017-01-07T02:18:42Z","timestamp":1483755522000},"page":"1718-1728","source":"Crossref","is-referenced-by-count":48,"title":["Intravital Imaging of Neutrophil Recruitment Reveals the Efficacy of FPR1 Blockade in Hepatic Ischemia-Reperfusion Injury"],"prefix":"10.1093","volume":"198","author":[{"given":"Masaki","family":"Honda","sequence":"first","affiliation":[{"name":"Department of Transplantation and Pediatric Surgery, Postgraduate School of Medical Sciences, Kumamoto University , Kumamoto 860-8556,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6102-3201","authenticated-orcid":false,"given":"Takayuki","family":"Takeichi","sequence":"additional","affiliation":[{"name":"Department of Transplantation and Pediatric Surgery, Postgraduate School of Medical Sciences, Kumamoto University , Kumamoto 860-8556,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shintaro","family":"Hashimoto","sequence":"additional","affiliation":[{"name":"Department of Transplantation and Pediatric Surgery, Postgraduate School of Medical Sciences, Kumamoto University , Kumamoto 860-8556,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daiki","family":"Yoshii","sequence":"additional","affiliation":[{"name":"Department of Transplantation and Pediatric Surgery, Postgraduate School of Medical Sciences, Kumamoto University , Kumamoto 860-8556,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaori","family":"Isono","sequence":"additional","affiliation":[{"name":"Department of Transplantation and Pediatric Surgery, Postgraduate School of Medical Sciences, Kumamoto University , Kumamoto 860-8556,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shintaro","family":"Hayashida","sequence":"additional","affiliation":[{"name":"Department of Transplantation and Pediatric Surgery, Postgraduate School of Medical Sciences, Kumamoto University , Kumamoto 860-8556,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuki","family":"Ohya","sequence":"additional","affiliation":[{"name":"Department of Transplantation and Pediatric Surgery, Postgraduate School of Medical Sciences, Kumamoto University , Kumamoto 860-8556,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hidekazu","family":"Yamamoto","sequence":"additional","affiliation":[{"name":"Department of Transplantation and Pediatric Surgery, Postgraduate School of Medical Sciences, Kumamoto University , Kumamoto 860-8556,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasuhiko","family":"Sugawara","sequence":"additional","affiliation":[{"name":"Department of Transplantation and Pediatric Surgery, Postgraduate School of Medical Sciences, Kumamoto University , Kumamoto 860-8556,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7477-9614","authenticated-orcid":false,"given":"Yukihiro","family":"Inomata","sequence":"additional","affiliation":[{"name":"Department of Transplantation and Pediatric Surgery, Postgraduate School of Medical Sciences, Kumamoto University , Kumamoto 860-8556,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2017,2,15]]},"reference":[{"key":"2025030615034143900_r1","doi-asserted-by":"crossref","first-page":"1563","DOI":"10.1111\/j.1600-6143.2011.03579.x","article-title":"Liver ischemia and reperfusion injury: new insights into mechanisms of innate-adaptive immune-mediated tissue inflammation","volume":"11","author":"Zhai","year":"2011","journal-title":"Am. 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