| Chemokine receptor CXCR2 mediates bacterial clearance rather than neutrophil recruitment in a murine model of pneumonic plague. | |
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MedLine Citation:
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PMID: 21356370 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Pulmonary infection by Yersinia pestis causes pneumonic plague, a necrotic bronchopneumonia that is rapidly lethal and highly contagious. Acute pneumonic plague accompanies the up-regulation of pro-inflammatory cytokines and chemokines, suggesting that the host innate immune response may contribute to the development of disease. To address this possibility, we sought to understand the consequences of neutrophil recruitment during pneumonic plague, and we studied the susceptibility of C3H-HeN mice lacking the CXC chemokine KC or its receptor CXC receptor 2 (CXCR2) to pulmonary Y. pestis infection. We found that without Kc or Cxcr2, disease progression was accelerated both in bacterial growth and development of primary bronchopneumonia. When examined in an antibody clearance model, Cxcr2(-/-) mice were not protected by neutralizing Y. pestis antibodies, yet bacterial growth in the lungs was delayed in a manner associated with a neutrophil-mediated inflammatory response. After this initial delay, however, robust neutrophil recruitment in Cxcr2(-/-) mice correlated with bacterial growth and the development of fulminant pneumonic and septicemic plague. In contrast, attenuated Y. pestis lacking the conserved pigmentation locus could be cleared from the lungs in the absence of Cxcr2 indicating virulence factors within this locus may inhibit CXCR2-independent pathways of bacterial killing. Together, the data suggest CXCR2 uniquely induces host defense mechanisms that are effective against virulent Y. pestis, raising new insight into the activation of neutrophils during infection. |
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Authors:
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Nicholas A Eisele; Hanni Lee-Lewis; Cynthia Besch-Williford; Charles R Brown; Deborah M Anderson |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: The American journal of pathology Volume: 178 ISSN: 1525-2191 ISO Abbreviation: Am. J. Pathol. Publication Date: 2011 Mar |
Date Detail:
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Created Date: 2011-03-01 Completed Date: 2011-05-25 Revised Date: 2012-03-01 |
Medline Journal Info:
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Nlm Unique ID: 0370502 Medline TA: Am J Pathol Country: United States |
Other Details:
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Languages: eng Pagination: 1190-200 Citation Subset: AIM; IM |
Copyright Information:
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Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri 65211, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antibodies, Bacterial / immunology Antigens, Bacterial / immunology Chemokine CXCL1 / metabolism Disease Models, Animal Disease Progression Lung / immunology, microbiology, pathology Mice Models, Immunological Mutation / genetics Neutrophil Infiltration / immunology* Plague / immunology*, microbiology*, prevention & control Pore Forming Cytotoxic Proteins / immunology Receptors, Interleukin-8B / metabolism* Signal Transduction Yersinia pestis / growth & development, immunology* |
| Grant Support | |
ID/Acronym/Agency:
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T32 GM008396/GM/NIGMS NIH HHS; T32 RR007004/RR/NCRR NIH HHS; U54 AI157160/AI/NIAID NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antibodies, Bacterial; 0/Antigens, Bacterial; 0/Chemokine CXCL1; 0/Cxcl1 protein, mouse; 0/LcrV protein, Yersinia; 0/Pore Forming Cytotoxic Proteins; 0/Receptors, Interleukin-8B |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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