Source:http://linkedlifedata.com/resource/pubmed/id/17095647
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2007-3-7
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pubmed:abstractText |
Leukocyte infiltration, mediated by chemokines, is a key step in the development of organ dysfunction. Lung and liver neutrophil infiltration following trauma-hemorrhage is associated with upregulation of monocyte chemoattractant protein-1 (MCP-1). Because MCP-1 is not a major attractant for neutrophils, we hypothesized that MCP-1 influences neutrophil infiltration via regulation of keratinocyte-derived chemokines (KC). To study this, male C3H/HeN mice were pretreated with MCP-1 antiserum or control serum and subjected to trauma-hemorrhage or sham operation. Animals were killed 4 h after resuscitation. One group of trauma-hemorrhage mice receiving MCP-1 antiserum was also treated with murine KC during resuscitation. Plasma levels and tissue content of MCP-1 and KC were determined by cytometric bead arrays. Immunohistochemistry was performed to determine neutrophil infiltration; organ damage was assessed by edema formation. Treatment with MCP-1 antiserum significantly decreased systemic, lung, and liver levels of MCP-1 and KC following trauma-hemorrhage. This decrease in MCP-1 levels was associated with decreased neutrophil infiltration and edema formation in lung and liver following trauma-hemorrhage. Restitution of KC in mice treated with MCP-1 antiserum restored tissue neutrophil infiltration and edema. These results lead us to conclude that increased levels of MCP-1 cause neutrophil accumulation and distant organ damage by regulating KC production during the postinjury inflammatory response.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0363-6119
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
292
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
R1110-6
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pubmed:dateRevised |
2007-12-3
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pubmed:meshHeading |
pubmed-meshheading:17095647-Animals,
pubmed-meshheading:17095647-Chemokine CCL2,
pubmed-meshheading:17095647-Chemokines,
pubmed-meshheading:17095647-Edema,
pubmed-meshheading:17095647-Gene Expression Regulation,
pubmed-meshheading:17095647-Hemorrhage,
pubmed-meshheading:17095647-Immunohistochemistry,
pubmed-meshheading:17095647-Keratinocytes,
pubmed-meshheading:17095647-Liver,
pubmed-meshheading:17095647-Lung,
pubmed-meshheading:17095647-Male,
pubmed-meshheading:17095647-Mice,
pubmed-meshheading:17095647-Mice, Inbred C3H,
pubmed-meshheading:17095647-Neutrophil Infiltration,
pubmed-meshheading:17095647-Time Factors,
pubmed-meshheading:17095647-Wounds and Injuries
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pubmed:year |
2007
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pubmed:articleTitle |
Monocyte chemoattractant protein-1 influences trauma-hemorrhage-induced distal organ damage via regulation of keratinocyte-derived chemokine production.
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pubmed:affiliation |
Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Volker Hall-Suite G094, 1670 University Blvd., Birmingham, AL 35294-0019, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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