期刊
CRITICAL CARE MEDICINE
卷 37, 期 4, 页码 1389-1396出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/CCM.0b013e31819ceb71
关键词
adhesion; neutrophils; platelets; lung; sepsis
资金
- Swedish Medical Research Council [2006-4889]
- Crafoordska stiftelsen
- Einar och Inga Nilssons stiftelse
- Harald och Greta Jaenssons stiftelse
- Greta och Johan Kocks stiftelser
- Froken Agnes Nilssons stiftelse
- Franke och Margareta Bergqvists stiftelse for framjande av cancerforskning
- Magnus Bergvalls stiftelse
- Mossfelts stiftelse
- Nanna Svartz stiftelse
- Ruth och Richard Julins stiftelse
- Svenska Lakaresallskapet
- Allmana sjukhusets i Malmo stiftelse for bekampande av cancer
- MAS fonder
- Malmo University Hospita
- Lund University
Objective. Recent findings Indicate that platelets not only regulate thrombosis and hemostasis but may also be involved in proinflammatory activities. Herein, we hypothesized that platelets may play a role in sepsis by activating and priming circulating neutrophils for subsequent recruitment Into the lung. Design: Prospective experimental study. Setting. University Hospital Research Unit. Subject. Male C57BL/6 mice. Interventions. Lung edema, bronchoalveolar infiltration of neutrophils, levels of myeloperoxidase, expression and function of membrane-activated complex-1 (Mac-1) on neutrophils and the CXC chemokines, macrophage inflammatory protein-2, and cytokine-induced neutrophil chemoattractant were determined after cecal ligation and puncture (CLP). Mice received a platelet-depleting antibody as well as antibodies directed against P-selectin glycoprotein-ligand-1 and Mac-1 before CLP induction. Measurements and Main Results. CLP caused significant pulmonary damage characterized by neutrophil infiltration, increased levels of CXC chemokines, and edema formation in the lung. Furthermore, CLP up-regulated Mac-1 expression on neutrophils and increased the number of neutrophils binding platelets in the circulation. Interestingly, depletion of platelets reduced CLP-induced edema and neutrophil recruitment in the bronchoalveolar space by >60%. Furthermore, depletion of platelets reduced Mac-1 expression on neutrophils. On the other hand, inhibition of P-selectin glycoprotein-ligand-1 abolished CLP-induced neutrophil-platelet aggregation but had no effect on neutrophil expression of Mac-1. Conclusions: These data demonstrate that platelets play a key role in regulating infiltration of neutrophils and edema formation in the lung via upregulation of Mac-1 in abdominal sepsis. (Crit Care Med 2009; 37:1389-1396)
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