| Mechanism of neutrophil recruitment to the lung after pulmonary contusion. | |
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MedLine Citation:
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PMID: 21330942 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Blunt chest trauma resulting in pulmonary contusion is a common but poorly understood injury. We previously demonstrated that lung contusion activates localized and systemic innate immune mechanisms and recruits neutrophils to the injured lung. We hypothesized that the innate immune and inflammatory activation of neutrophils may figure prominently in the response to lung injury. To investigate this, we used a model of pulmonary contusion in the mouse that is similar to that observed clinically in humans and evaluated postinjury lung function and pulmonary neutrophil recruitment. Comparisons were made between injured mice with and without neutrophil depletion. We further examined the role of chemokines and adhesion receptors in neutrophil recruitment to the injured lung. We found that lung injury and resultant physiological dysfunction after contusion were dependent on the presence of neutrophils in the alveolar space. We show that CXCL1, CXCL2/3, and CXCR2 are involved in neutrophil recruitment to the lung after injury and that intercellular adhesion molecule 1 is locally expressed and actively participates in this process. Injured gp91-deficient mice showed improved lung function, indicating that oxidant production by neutrophil NADPH oxidase mediates lung dysfunction after contusion. These data suggest that both neutrophil presence and function are required for lung injury after lung contusion. |
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Authors:
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J Jason Hoth; Jonathan D Wells; Elizabeth M Hiltbold; Charles E McCall; Barbara K Yoza |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Shock (Augusta, Ga.) Volume: 35 ISSN: 1540-0514 ISO Abbreviation: Shock Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-05-17 Completed Date: 2011-09-02 Revised Date: 2011-11-30 |
Medline Journal Info:
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Nlm Unique ID: 9421564 Medline TA: Shock Country: United States |
Other Details:
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Languages: eng Pagination: 604-9 Citation Subset: IM |
Affiliation:
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Department of General Surgery, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157, USA. jhoth@wfubmc.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Chemokine CXCL1 / physiology Chemokine CXCL2 / physiology Chemokines, CXC / physiology Intercellular Adhesion Molecule-1 / physiology Lung / immunology*, physiopathology Lung Injury / immunology*, physiopathology* Membrane Glycoproteins / deficiency Mice NADPH Oxidase / deficiency Neutrophil Infiltration / immunology* Receptors, Interleukin-8B / physiology Wounds, Nonpenetrating / immunology |
| Grant Support | |
ID/Acronym/Agency:
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AI057770/AI/NIAID NIH HHS; AI065791/AI/NIAID NIH HHS; GM083154/GM/NIGMS NIH HHS; R01 AI065791-06/AI/NIAID NIH HHS; R01 AI065791-07/AI/NIAID NIH HHS; R01 AI079144-02/AI/NIAID NIH HHS; R01 AI079144-03/AI/NIAID NIH HHS; RR023570/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Chemokine CXCL1; 0/Chemokine CXCL2; 0/Chemokines, CXC; 0/Cxcl1 protein, mouse; 0/Cxcl2 protein, mouse; 0/Membrane Glycoproteins; 0/Receptors, Interleukin-8B; 126547-89-5/Intercellular Adhesion Molecule-1; EC 1.6.3.1/Cybb protein, mouse; EC 1.6.3.1/NADPH Oxidase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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