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CINC-1 is identified as an acute-phase protein induced by focal brain injury causing leukocyte mobilization and liver injury

CINC-1 is identified as an acute-phase protein induced by focal brain injury causing leukocyte mobilization and liver injury
CINC-1 is identified as an acute-phase protein induced by focal brain injury causing leukocyte mobilization and liver injury
Following injury or infection, the liver releases acute-phase proteins (APP). After a severe focal injury, this systemic response can be excessive and may lead to multiorgan dysfunction (MODS). CINC-1 is a neutrophil chemoattractant, and we have now established that it also functions as an early APP after injury to the brain or to peripheral tissues. After induction of a focal inflammatory lesion in the brain, there is rapid hepatic and serum CINC-1 induction, which is associated with increases in neutrophil numbers within the liver and within the circulation. CINC-1-mediated recruitment of neutrophils to organs distant from the primary injury site may contribute to MODS. Indeed, we found that enzyme markers of liver tissue injury are increased in the serum following generation of a focal inflammatory lesion in the brain. Neutralization of CINC-1 in the periphery reversed brain-injury-induced neutrophil mobilization and inhibited recruitment of neutrophils to the brain and to the liver. Thus, a significant component of the hepatic acute-phase response is the release of chemokines by the liver, which act to amplify the inflammatory response and modulate the subsequent leukocytosis and secondary tissue damage. Hepatic CINC-1 synthesis following injury presents a novel focus for treatment of inflammation.
mods, IL-1?, cytokine, chemokine, neutrophil
0892-6638
1168-1170
Campbell, Sandra J.
5c85ee6c-22f6-47d9-9e11-21173a9323a5
Hughes, Paula M.
eb8721bf-bb7f-467b-a9e9-729a7ddcd2e3
Iredale, John P.
607673ce-77b2-4418-b317-2aa778110ee2
Wilcockson, David C.
ba84a5a7-c06c-4d54-ba4d-1113c607e28e
Waters, Sara
98d640df-c057-462a-afb6-8ddecdc11c41
Docagne, Fabian
844cc8bb-9eb2-47c0-b41e-1025d4527633
Perry, V. Hugh
8f29d36a-8e1f-4082-8700-09483bbaeae4
Anthony, Daniel C.
928249fa-dcf4-4088-b95b-ce14c719164d
Campbell, Sandra J.
5c85ee6c-22f6-47d9-9e11-21173a9323a5
Hughes, Paula M.
eb8721bf-bb7f-467b-a9e9-729a7ddcd2e3
Iredale, John P.
607673ce-77b2-4418-b317-2aa778110ee2
Wilcockson, David C.
ba84a5a7-c06c-4d54-ba4d-1113c607e28e
Waters, Sara
98d640df-c057-462a-afb6-8ddecdc11c41
Docagne, Fabian
844cc8bb-9eb2-47c0-b41e-1025d4527633
Perry, V. Hugh
8f29d36a-8e1f-4082-8700-09483bbaeae4
Anthony, Daniel C.
928249fa-dcf4-4088-b95b-ce14c719164d

Campbell, Sandra J., Hughes, Paula M., Iredale, John P., Wilcockson, David C., Waters, Sara, Docagne, Fabian, Perry, V. Hugh and Anthony, Daniel C. (2003) CINC-1 is identified as an acute-phase protein induced by focal brain injury causing leukocyte mobilization and liver injury. FASEB Journal, 17 (9), 1168-1170. (doi:10.1096/fj.02-0757fje).

Record type: Article

Abstract

Following injury or infection, the liver releases acute-phase proteins (APP). After a severe focal injury, this systemic response can be excessive and may lead to multiorgan dysfunction (MODS). CINC-1 is a neutrophil chemoattractant, and we have now established that it also functions as an early APP after injury to the brain or to peripheral tissues. After induction of a focal inflammatory lesion in the brain, there is rapid hepatic and serum CINC-1 induction, which is associated with increases in neutrophil numbers within the liver and within the circulation. CINC-1-mediated recruitment of neutrophils to organs distant from the primary injury site may contribute to MODS. Indeed, we found that enzyme markers of liver tissue injury are increased in the serum following generation of a focal inflammatory lesion in the brain. Neutralization of CINC-1 in the periphery reversed brain-injury-induced neutrophil mobilization and inhibited recruitment of neutrophils to the brain and to the liver. Thus, a significant component of the hepatic acute-phase response is the release of chemokines by the liver, which act to amplify the inflammatory response and modulate the subsequent leukocytosis and secondary tissue damage. Hepatic CINC-1 synthesis following injury presents a novel focus for treatment of inflammation.

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More information

Published date: 22 April 2003
Additional Information: FASEB Journal express article
Keywords: mods, IL-1?, cytokine, chemokine, neutrophil
Organisations: Biological Sciences

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Local EPrints ID: 56605
URI: http://eprints.soton.ac.uk/id/eprint/56605
ISSN: 0892-6638
PURE UUID: e8a4182b-3cf2-40ce-b6a3-b0b1f9527915

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Date deposited: 11 Aug 2008
Last modified: 07 Jan 2022 22:32

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Contributors

Author: Sandra J. Campbell
Author: Paula M. Hughes
Author: John P. Iredale
Author: David C. Wilcockson
Author: Sara Waters
Author: Fabian Docagne
Author: V. Hugh Perry
Author: Daniel C. Anthony

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