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Interleukin-6 mediates neutrophil mobilization from bone marrow in pulmonary hypertension

Cellular & Molecular Immunology 2021年第2期18卷 374-384页

作者： Jonathan Florentin Jingsi Zhao Yi-Yin Tai Sathish Babu Vasamsetti Scott P.O’Neil Rahul Kumar Anagha Arunkumar Annie Watson john sembrat Grant C.Bullock Linda Sanders Biruk Kassa Mauricio Rojas Brian B.Graham Stephen Y.Chan Partha Dutta Center for Pulmonary Vascular Biology and Medicine Pittsburgh HeartLungBloodand Vascular Medicine InstituteDivision of CardiologyDepartment of MedicineUniversity of Pittsburgh School of MedicineUniversity of Pittsburgh Medical CenterPittsburghPA15213USA Division of Pulmonary and Critical Care Medicine Zuckerberg San Francisco General Hospital and Trauma CenterUniversity of California San FranciscoBuilding 1002nd floor1001 Potrero AveSan FranciscoCAUSA Division of Pulmonary Allergy and Critical Care MedicineUniversity of PittsburghPittsburghPA15261USA Division of Hematopathology Pittsburgh HeartLungBloodand Vascular Medicine Institute University of Pittsburgh School of MedicineUniversity of Pittsburgh Medical CenterPittsburghPA15213USA Department of Medicine Anschutz Medical CampusBuilding RC29th floor12700 E 19th AveAuroraCO80045USA Department of Immunology University of Pittsburgh School of MedicinePittsburghPA15213USA

Myeloid cells,such as neutrophils,are produced in the bone marrow in high quantities and are important in the pathogenesis of vascular diseases such as pulmonary hypertension(PH).Although neutrophil recruitment into sites of inflammation has been well studied,the mechanisms of neutrophil egress from the bone marrow are not well *** computational flow cytometry,we observed increased neutrophils in the lungs of patients and mice with ***,we found elevated levels of IL-6 in the blood and lungs of patients and mice with *** observed that transgenic mice overexpressing Il-6 in the lungs displayed elevated neutrophil egress from the bone marrow and exaggerated neutrophil recruitment to the lungs,resulting in exacerbated pulmonary vascular remodeling,and dysfunctional ***,we found that IL-6-induced neutrophil egress from the bone marrow was dependent on interferon regulatory factor 4(IRF-4)-mediated CX3CR1 expression in ***,Cx3cr1 genetic deficiency in hematopoietic cells in Il-6-transgenic mice significantly reduced neutrophil egress from bone marrow and decreased neutrophil counts in the lungs,thus ameliorating pulmonary remodeling and *** summary,these findings define a novel mechanism of IL-6-induced neutrophil egress from the bone marrow and reveal a new therapeutic target to curtail neutrophil-mediated inflammation in pulmonary vascular disease.

关键词： neutrophil IL-6 pulmonary hypertension CX3CR1 inflammation

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