The effect of inflammation on coagulation and vice versa
PURPOSE OF REVIEWIn infection, inflammation is frequently accompanied by a disturbance of the normal hemostatic balance provided by procoagulant and anticoagulant mechanisms. This review summarizes recently acquired knowledge on the bimodal interactions between coagulation and inflammation in infect...
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Veröffentlicht in: | Current opinion in infectious diseases 2011-06, Vol.24 (3), p.273-278 |
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description | PURPOSE OF REVIEWIn infection, inflammation is frequently accompanied by a disturbance of the normal hemostatic balance provided by procoagulant and anticoagulant mechanisms. This review summarizes recently acquired knowledge on the bimodal interactions between coagulation and inflammation in infection.
RECENT FINDINGSInfection elicits inflammation-induced coagulation via tissue factor. A net procoagulant state is further produced by impaired functioning of anticoagulant mechanisms among which is the protein C system. Protease activated receptors (PARs) form the molecular link between coagulation and inflammation. PAR1 mediates both detrimental (induced by thrombin) and protective (induced by activated protein C) cellular effects. Activated protein C protects against mortality in experimental endotoxemia and sepsis by effects that rely on PAR1, not on the anticoagulant properties of this protein.
SUMMARYRecent data provide new insights into how inflammation impacts on coagulation and vice versa, identifying crucial roles for PARs. This knowledge may assist in designing novel interventions targeted at the perpetuation of inflammation by mediators traditionally implicated in coagulation. |
doi_str_mv | 10.1097/QCO.0b013e328344c078 |
format | Article |
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RECENT FINDINGSInfection elicits inflammation-induced coagulation via tissue factor. A net procoagulant state is further produced by impaired functioning of anticoagulant mechanisms among which is the protein C system. Protease activated receptors (PARs) form the molecular link between coagulation and inflammation. PAR1 mediates both detrimental (induced by thrombin) and protective (induced by activated protein C) cellular effects. Activated protein C protects against mortality in experimental endotoxemia and sepsis by effects that rely on PAR1, not on the anticoagulant properties of this protein.
SUMMARYRecent data provide new insights into how inflammation impacts on coagulation and vice versa, identifying crucial roles for PARs. This knowledge may assist in designing novel interventions targeted at the perpetuation of inflammation by mediators traditionally implicated in coagulation.</description><identifier>ISSN: 0951-7375</identifier><identifier>EISSN: 1473-6527</identifier><identifier>DOI: 10.1097/QCO.0b013e328344c078</identifier><identifier>PMID: 21330919</identifier><language>eng</language><publisher>United States: Lippincott Williams & Wilkins, Inc</publisher><subject>Blood Coagulation Disorders - physiopathology ; Communicable Diseases - pathology ; Humans ; Inflammation - physiopathology ; Receptors, Proteinase-Activated - metabolism</subject><ispartof>Current opinion in infectious diseases, 2011-06, Vol.24 (3), p.273-278</ispartof><rights>2011 Lippincott Williams & Wilkins, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4218-5f1d11528112b60034ed93c3732071b30fa50661567f7b5c71a65ec43da44dcf3</citedby><cites>FETCH-LOGICAL-c4218-5f1d11528112b60034ed93c3732071b30fa50661567f7b5c71a65ec43da44dcf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21330919$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van der Poll, Tom</creatorcontrib><creatorcontrib>Boer, Johannes Daan de</creatorcontrib><creatorcontrib>Levi, Marcel</creatorcontrib><title>The effect of inflammation on coagulation and vice versa</title><title>Current opinion in infectious diseases</title><addtitle>Curr Opin Infect Dis</addtitle><description>PURPOSE OF REVIEWIn infection, inflammation is frequently accompanied by a disturbance of the normal hemostatic balance provided by procoagulant and anticoagulant mechanisms. This review summarizes recently acquired knowledge on the bimodal interactions between coagulation and inflammation in infection.
RECENT FINDINGSInfection elicits inflammation-induced coagulation via tissue factor. A net procoagulant state is further produced by impaired functioning of anticoagulant mechanisms among which is the protein C system. Protease activated receptors (PARs) form the molecular link between coagulation and inflammation. PAR1 mediates both detrimental (induced by thrombin) and protective (induced by activated protein C) cellular effects. Activated protein C protects against mortality in experimental endotoxemia and sepsis by effects that rely on PAR1, not on the anticoagulant properties of this protein.
SUMMARYRecent data provide new insights into how inflammation impacts on coagulation and vice versa, identifying crucial roles for PARs. This knowledge may assist in designing novel interventions targeted at the perpetuation of inflammation by mediators traditionally implicated in coagulation.</description><subject>Blood Coagulation Disorders - physiopathology</subject><subject>Communicable Diseases - pathology</subject><subject>Humans</subject><subject>Inflammation - physiopathology</subject><subject>Receptors, Proteinase-Activated - metabolism</subject><issn>0951-7375</issn><issn>1473-6527</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1Lw0AQhhdRbK3-A5HcPKXO7Ed2c5TiFxSKUM9hs9m10U1Ss0mL_95IqgcPwsAw8LwzzEPIJcIcIZU3z4vVHHJAZhlVjHMDUh2RKXLJ4kRQeUymkAqMJZNiQs5CeANAmkJySiYUGYMU0ylR642NrHPWdFHjorJ2XleV7sqmjoYyjX7t_Tjquoh2pbHRzrZBn5MTp32wF4c-Iy_3d-vFY7xcPTwtbpex4RRVLBwWiIIqRJonAIzbImWGSUZBYs7AaQFJgiKRTubCSNSJsIazQnNeGMdm5Hrcu22bj96GLqvKYKz3urZNHzKVME6VAjaQfCRN24TQWpdt27LS7WeGkH0rywZl2V9lQ-zqcKDPK1v8hn4cDYAagX3ju-H1d9_vbZttrPbd5v_dX5Bid7E</recordid><startdate>201106</startdate><enddate>201106</enddate><creator>van der Poll, Tom</creator><creator>Boer, Johannes Daan de</creator><creator>Levi, Marcel</creator><general>Lippincott Williams & Wilkins, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201106</creationdate><title>The effect of inflammation on coagulation and vice versa</title><author>van der Poll, Tom ; Boer, Johannes Daan de ; Levi, Marcel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4218-5f1d11528112b60034ed93c3732071b30fa50661567f7b5c71a65ec43da44dcf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Blood Coagulation Disorders - physiopathology</topic><topic>Communicable Diseases - pathology</topic><topic>Humans</topic><topic>Inflammation - physiopathology</topic><topic>Receptors, Proteinase-Activated - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van der Poll, Tom</creatorcontrib><creatorcontrib>Boer, Johannes Daan de</creatorcontrib><creatorcontrib>Levi, Marcel</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Current opinion in infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van der Poll, Tom</au><au>Boer, Johannes Daan de</au><au>Levi, Marcel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The effect of inflammation on coagulation and vice versa</atitle><jtitle>Current opinion in infectious diseases</jtitle><addtitle>Curr Opin Infect Dis</addtitle><date>2011-06</date><risdate>2011</risdate><volume>24</volume><issue>3</issue><spage>273</spage><epage>278</epage><pages>273-278</pages><issn>0951-7375</issn><eissn>1473-6527</eissn><abstract>PURPOSE OF REVIEWIn infection, inflammation is frequently accompanied by a disturbance of the normal hemostatic balance provided by procoagulant and anticoagulant mechanisms. This review summarizes recently acquired knowledge on the bimodal interactions between coagulation and inflammation in infection.
RECENT FINDINGSInfection elicits inflammation-induced coagulation via tissue factor. A net procoagulant state is further produced by impaired functioning of anticoagulant mechanisms among which is the protein C system. Protease activated receptors (PARs) form the molecular link between coagulation and inflammation. PAR1 mediates both detrimental (induced by thrombin) and protective (induced by activated protein C) cellular effects. Activated protein C protects against mortality in experimental endotoxemia and sepsis by effects that rely on PAR1, not on the anticoagulant properties of this protein.
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subjects | Blood Coagulation Disorders - physiopathology Communicable Diseases - pathology Humans Inflammation - physiopathology Receptors, Proteinase-Activated - metabolism |
title | The effect of inflammation on coagulation and vice versa |
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