Document Detail


Functional contribution of CXCR2 to lung injury after aspiration of acid and gastric particulates.
MedLine Citation:
PMID:  20044435     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The effects of individual ELR+ CXC chemokines have been documented in experimental models of acid aspiration. However, aspiration lung injury would be influenced by the combined effects of these chemokines and other factors related to their function. Therefore, the role of the chemokine receptor CXCR2 was examined in lung injury induced by aspiration of acid and acid with gastric particulates. Anesthetized mice were given intratracheal injections of saline, acid solution, or acid containing gastric particles. Within 6 h, bronchoalveolar lavage fluid neutrophils and albumin increased relative to the severity of the insult. Immunohistochemistry and RT-PCR demonstrated striking increases in pulmonary expression of CXCR2 after aspiration. In CXCR2-deficient mice, neutrophil recruitment to airways was significantly reduced after aspiration of either acid or acid with particles. However, lung injury scores were unaffected in Ccr2-/- mice in the acid + particles group. Esterase-stained lung tissue demonstrated that focal aggregates of inflammatory cells contained neutrophils in the Ccr2-/- mice. These studies suggest CXCR2 and its ligands are dominant mediators of neutrophil recruitment to airways after aspiration. However, CXCR2-independent mechanisms recruit neutrophils into areas of cellular aggregation after aspiration of acidified gastric particulates.
Authors:
Jean A Nemzek; Omorodola Abatan; Christopher Fry; Aladdein Mattar
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-12-31
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  298     ISSN:  1522-1504     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-02-24     Completed Date:  2010-03-17     Revised Date:  2011-07-25    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L382-91     Citation Subset:  IM    
Affiliation:
Unit for Laboratory Animal Medicine, Department of Pathology, University of Michigan, 1150 W. Medical Center Drive, Ann Arbor, MI 48109, USA. jnemzek@umich.edu
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MeSH Terms
Descriptor/Qualifier:
Acids
Animals
Antibodies, Neutralizing / pharmacology
Bronchoalveolar Lavage Fluid / cytology
Chemokines / metabolism
Female
Gene Expression Regulation / drug effects
Leukocyte Count
Lung / drug effects,  metabolism
Lung Injury / complications*,  metabolism,  pathology*
Mice
Mice, Inbred ICR
Neutrophils / cytology,  drug effects,  metabolism
Particulate Matter / adverse effects*
Pneumonia / metabolism,  pathology
RNA, Messenger / genetics,  metabolism
Receptors, Interleukin-8B / deficiency,  genetics,  metabolism*
Respiratory Aspiration / complications*,  pathology*
Stomach / metabolism*
Grant Support
ID/Acronym/Agency:
K08-GM-065486/GM/NIGMS NIH HHS; P01-GM-067189/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Acids; 0/Antibodies, Neutralizing; 0/Chemokines; 0/Particulate Matter; 0/RNA, Messenger; 0/Receptors, Interleukin-8B
Comments/Corrections

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