{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mizuno T"],"funding":["Research Center for Pathogenesis of Intractable Diseases, Research Institute of Meijo University","Ministry of Education, Culture, Science, and Technology","Japan Society for the Promotion of Science"],"pagination":["574-583"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10988669"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(4)"],"pubmed_abstract":["Acute lung injury (ALI), which occurs in association with sepsis, trauma, and coronavirus disease 2019 (COVID-19), is a serious clinical condition with high mortality. Excessive platelet-leukocyte aggregate (PLA) formation promotes neutrophil extracellular trap (NET) release and thrombosis, which are involved in various diseases, including ALI. Macrophage-1 antigen (Mac-1, CD11b/CD18), which is expressed on the surface of leukocytes, is known to promote NET formation. This study aimed to elucidate the role of Mac-1 in extracellular histone-induced ALI. Exogenous histones were administered to Mac-1-deficient mice and wild-type (WT) mice with or without neutrophil or platelet depletion, and several parameters were investigated 1 h after histone injection. Depletion of neutrophils or platelets improved survival time and macroscopic and microscopic properties of lung tissues, and decreased platelet-leukocyte formation and plasma myeloperoxidase levels. These improvements were also observed in Mac-1<sup>-/-</sup> mice. NET formation in Mac-1<sup>-/-</sup> bone marrow neutrophils (BMNs) was significantly lower than that in WT BMNs. In conclusion, our findings suggest that Mac-1 is associated with exacerbation of histone-induced ALI and the promotion of NET formation in the presence of activated platelets."],"journal":["FEBS open bio"],"pubmed_title":["Macrophage-1 antigen exacerbates histone-induced acute lung injury and promotes neutrophil extracellular trap formation."],"pmcid":["PMC10988669"],"funding_grant_id":["19K07232","21K06696","20J22610"],"pubmed_authors":["Mizuno T","Nagano F","Fruhashi K","Yamada S","Tsuboi N","Takahashi K","Maruyama S"],"additional_accession":[]},"is_claimable":false,"name":"Macrophage-1 antigen exacerbates histone-induced acute lung injury and promotes neutrophil extracellular trap formation.","description":"Acute lung injury (ALI), which occurs in association with sepsis, trauma, and coronavirus disease 2019 (COVID-19), is a serious clinical condition with high mortality. Excessive platelet-leukocyte aggregate (PLA) formation promotes neutrophil extracellular trap (NET) release and thrombosis, which are involved in various diseases, including ALI. Macrophage-1 antigen (Mac-1, CD11b/CD18), which is expressed on the surface of leukocytes, is known to promote NET formation. This study aimed to elucidate the role of Mac-1 in extracellular histone-induced ALI. Exogenous histones were administered to Mac-1-deficient mice and wild-type (WT) mice with or without neutrophil or platelet depletion, and several parameters were investigated 1 h after histone injection. Depletion of neutrophils or platelets improved survival time and macroscopic and microscopic properties of lung tissues, and decreased platelet-leukocyte formation and plasma myeloperoxidase levels. These improvements were also observed in Mac-1<sup>-/-</sup> mice. NET formation in Mac-1<sup>-/-</sup> bone marrow neutrophils (BMNs) was significantly lower than that in WT BMNs. In conclusion, our findings suggest that Mac-1 is associated with exacerbation of histone-induced ALI and the promotion of NET formation in the presence of activated platelets.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2025-04-18T20:13:30.768Z","creation":"2025-04-07T08:07:17.189Z"},"accession":"S-EPMC10988669","cross_references":{"pubmed":["38360057"],"doi":["10.1002/2211-5463.13779"]}}