Interactions of leukocyte integrins with intercellular adhesion molecule 1 in the production of inflammatory vascular injury in vivo. The Shwartzman reaction revisited
We have investigated the role of leukocyte-endothelial cell interactions in a rabbit model of hemorrhagic vasculitis. Microvascular injury was produced in the skin by intradermal injection of Salmonella typhosa endotoxin followed 20 h later by intravenous zymosan, which activates complement. Hemorrh...
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Veröffentlicht in: | The Journal of clinical investigation 1992-01, Vol.89 (1), p.259-272 |
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description | We have investigated the role of leukocyte-endothelial cell interactions in a rabbit model of hemorrhagic vasculitis. Microvascular injury was produced in the skin by intradermal injection of Salmonella typhosa endotoxin followed 20 h later by intravenous zymosan, which activates complement. Hemorrhagic necrosis develops in the "prepared" skin sites which is characterized by microthrombi, neutrophil aggregation, platelet and fibrin deposition, and massive extravasation of erythrocytes. Hemorrhage in these Shwartzman-like lesions was quantitated by 99mTc-labeled autologous erythrocytes. Inhibition of the hemorrhagic response was obtained with mAb reactive with ICAM-1 as well as mAb against the leukocyte CD18 when either was administered intravenously just before intravenous zymosan challenge. This observation suggests that an intravascular event occurring in response to complement activation is required for the development of hemorrhagic vasculitis. We hypothesize that agents which successfully prepare the skin for the Shwartzman response after their intradermal injection do so by promoting increased intercellular adhesion molecule 1 (ICAM-1) expression on the vascular endothelium. Activation of complement then induces CD11/CD18 expression on circulating leukocytes thus producing an intravascular CD11/CD18-ICAM-1 (leukocyte-endothelium) adhesion event. Inhibition of intravascular leukocyte-leukocyte aggregation with mAb against CD11b (Mac-1) showed partial inhibition of hemorrhage, while mAb against CD11a (LFA-1) showed no inhibitory activity. This type of cytokine-primed, neutrophil-dependent vascular damage may be a model of human vasculitic processes where microvascular damage is produced in the absence of immune-complex deposition. |
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Inhibition of the hemorrhagic response was obtained with mAb reactive with ICAM-1 as well as mAb against the leukocyte CD18 when either was administered intravenously just before intravenous zymosan challenge. This observation suggests that an intravascular event occurring in response to complement activation is required for the development of hemorrhagic vasculitis. We hypothesize that agents which successfully prepare the skin for the Shwartzman response after their intradermal injection do so by promoting increased intercellular adhesion molecule 1 (ICAM-1) expression on the vascular endothelium. Activation of complement then induces CD11/CD18 expression on circulating leukocytes thus producing an intravascular CD11/CD18-ICAM-1 (leukocyte-endothelium) adhesion event. Inhibition of intravascular leukocyte-leukocyte aggregation with mAb against CD11b (Mac-1) showed partial inhibition of hemorrhage, while mAb against CD11a (LFA-1) showed no inhibitory activity. This type of cytokine-primed, neutrophil-dependent vascular damage may be a model of human vasculitic processes where microvascular damage is produced in the absence of immune-complex deposition.</description><identifier>ISSN: 0021-9738</identifier><identifier>DOI: 10.1172/JCI115570</identifier><identifier>PMID: 1345915</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Antibodies, Monoclonal - therapeutic use ; Antigens, CD - immunology ; Bacterial Toxins - pharmacology ; Blood Vessels - drug effects ; Blood Vessels - pathology ; Cell Adhesion - physiology ; Cell Adhesion Molecules - immunology ; Cell Adhesion Molecules - metabolism ; Cell Adhesion Molecules - toxicity ; Complement Activation ; Disease Models, Animal ; Endotoxins ; Enterotoxins - pharmacology ; Female ; Hemorrhage ; Integrins - metabolism ; Intercellular Adhesion Molecule-1 ; Leukocytes - metabolism ; Models, Biological ; Purpura, Schoenlein-Henoch - chemically induced ; Purpura, Schoenlein-Henoch - metabolism ; Purpura, Schoenlein-Henoch - therapy ; Rabbits ; Skin - drug effects ; Skin - pathology ; Zymosan - pharmacology</subject><ispartof>The Journal of clinical investigation, 1992-01, Vol.89 (1), p.259-272</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3390-b9d7d7151fb7e8c1ec9767864721265a9840d1eb2d9d64eb71194935acfab22f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC442844/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC442844/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1345915$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Argenbright, L W</creatorcontrib><creatorcontrib>Barton, R W</creatorcontrib><title>Interactions of leukocyte integrins with intercellular adhesion molecule 1 in the production of inflammatory vascular injury in vivo. The Shwartzman reaction revisited</title><title>The Journal of clinical investigation</title><addtitle>J Clin Invest</addtitle><description>We have investigated the role of leukocyte-endothelial cell interactions in a rabbit model of hemorrhagic vasculitis. Microvascular injury was produced in the skin by intradermal injection of Salmonella typhosa endotoxin followed 20 h later by intravenous zymosan, which activates complement. Hemorrhagic necrosis develops in the "prepared" skin sites which is characterized by microthrombi, neutrophil aggregation, platelet and fibrin deposition, and massive extravasation of erythrocytes. Hemorrhage in these Shwartzman-like lesions was quantitated by 99mTc-labeled autologous erythrocytes. Inhibition of the hemorrhagic response was obtained with mAb reactive with ICAM-1 as well as mAb against the leukocyte CD18 when either was administered intravenously just before intravenous zymosan challenge. This observation suggests that an intravascular event occurring in response to complement activation is required for the development of hemorrhagic vasculitis. We hypothesize that agents which successfully prepare the skin for the Shwartzman response after their intradermal injection do so by promoting increased intercellular adhesion molecule 1 (ICAM-1) expression on the vascular endothelium. Activation of complement then induces CD11/CD18 expression on circulating leukocytes thus producing an intravascular CD11/CD18-ICAM-1 (leukocyte-endothelium) adhesion event. Inhibition of intravascular leukocyte-leukocyte aggregation with mAb against CD11b (Mac-1) showed partial inhibition of hemorrhage, while mAb against CD11a (LFA-1) showed no inhibitory activity. This type of cytokine-primed, neutrophil-dependent vascular damage may be a model of human vasculitic processes where microvascular damage is produced in the absence of immune-complex deposition.</description><subject>Animals</subject><subject>Antibodies, Monoclonal - therapeutic use</subject><subject>Antigens, CD - immunology</subject><subject>Bacterial Toxins - pharmacology</subject><subject>Blood Vessels - drug effects</subject><subject>Blood Vessels - pathology</subject><subject>Cell Adhesion - physiology</subject><subject>Cell Adhesion Molecules - immunology</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Cell Adhesion Molecules - toxicity</subject><subject>Complement Activation</subject><subject>Disease Models, Animal</subject><subject>Endotoxins</subject><subject>Enterotoxins - pharmacology</subject><subject>Female</subject><subject>Hemorrhage</subject><subject>Integrins - metabolism</subject><subject>Intercellular Adhesion Molecule-1</subject><subject>Leukocytes - metabolism</subject><subject>Models, Biological</subject><subject>Purpura, Schoenlein-Henoch - chemically induced</subject><subject>Purpura, Schoenlein-Henoch - metabolism</subject><subject>Purpura, Schoenlein-Henoch - therapy</subject><subject>Rabbits</subject><subject>Skin - drug effects</subject><subject>Skin - pathology</subject><subject>Zymosan - pharmacology</subject><issn>0021-9738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkcFu1DAQhnMAlVJ64AGQfELisMXj2HF84IBWBRZV6oH2bDnOpHFJ4sV2Ui0vxGvi3a0KPdnj-b9_Rv6L4i3QCwDJPn5fbwCEkPRFcUopg5WSZf2qeB3jPaXAueAnxQmUXCgQp8WfzZQwGJucnyLxHRlw_untLiFxuXMXXH5-cKk_lMHiMMyDCcS0PcbMkNEPaOcBCWQFST2SbfDtfDDc-7mpG8w4muTDjiwm2gPupvs515lY3OIvyE3mfvQPJqTfo5lIwONG-bK46BK2b4qXnRkinj-eZ8Xtl8ub9bfV1fXXzfrz1cqWpaKrRrWylSCgayTWFtAqWcm64pIBq4RRNactYMNa1VYcGwmguCqFsZ1pGOvKs-LT0Xc7NyO2FqcUzKC3wY0m7LQ3Tj_vTK7Xd37RnLOa88y_f-SD_zVjTHp0cf9rZkI_Rw0VVExQmYUfjkIbfIwBu6cZQPU-SP0UZNa--3-pf8pjiuVfCAigdQ</recordid><startdate>199201</startdate><enddate>199201</enddate><creator>Argenbright, L W</creator><creator>Barton, R W</creator><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>7T5</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>199201</creationdate><title>Interactions of leukocyte integrins with intercellular adhesion molecule 1 in the production of inflammatory vascular injury in vivo. The Shwartzman reaction revisited</title><author>Argenbright, L W ; Barton, R W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3390-b9d7d7151fb7e8c1ec9767864721265a9840d1eb2d9d64eb71194935acfab22f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Animals</topic><topic>Antibodies, Monoclonal - therapeutic use</topic><topic>Antigens, CD - immunology</topic><topic>Bacterial Toxins - pharmacology</topic><topic>Blood Vessels - drug effects</topic><topic>Blood Vessels - pathology</topic><topic>Cell Adhesion - physiology</topic><topic>Cell Adhesion Molecules - immunology</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Cell Adhesion Molecules - toxicity</topic><topic>Complement Activation</topic><topic>Disease Models, Animal</topic><topic>Endotoxins</topic><topic>Enterotoxins - pharmacology</topic><topic>Female</topic><topic>Hemorrhage</topic><topic>Integrins - metabolism</topic><topic>Intercellular Adhesion Molecule-1</topic><topic>Leukocytes - metabolism</topic><topic>Models, Biological</topic><topic>Purpura, Schoenlein-Henoch - chemically induced</topic><topic>Purpura, Schoenlein-Henoch - metabolism</topic><topic>Purpura, Schoenlein-Henoch - therapy</topic><topic>Rabbits</topic><topic>Skin - drug effects</topic><topic>Skin - pathology</topic><topic>Zymosan - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Argenbright, L W</creatorcontrib><creatorcontrib>Barton, R W</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Argenbright, L W</au><au>Barton, R W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interactions of leukocyte integrins with intercellular adhesion molecule 1 in the production of inflammatory vascular injury in vivo. The Shwartzman reaction revisited</atitle><jtitle>The Journal of clinical investigation</jtitle><addtitle>J Clin Invest</addtitle><date>1992-01</date><risdate>1992</risdate><volume>89</volume><issue>1</issue><spage>259</spage><epage>272</epage><pages>259-272</pages><issn>0021-9738</issn><abstract>We have investigated the role of leukocyte-endothelial cell interactions in a rabbit model of hemorrhagic vasculitis. Microvascular injury was produced in the skin by intradermal injection of Salmonella typhosa endotoxin followed 20 h later by intravenous zymosan, which activates complement. Hemorrhagic necrosis develops in the "prepared" skin sites which is characterized by microthrombi, neutrophil aggregation, platelet and fibrin deposition, and massive extravasation of erythrocytes. Hemorrhage in these Shwartzman-like lesions was quantitated by 99mTc-labeled autologous erythrocytes. Inhibition of the hemorrhagic response was obtained with mAb reactive with ICAM-1 as well as mAb against the leukocyte CD18 when either was administered intravenously just before intravenous zymosan challenge. This observation suggests that an intravascular event occurring in response to complement activation is required for the development of hemorrhagic vasculitis. We hypothesize that agents which successfully prepare the skin for the Shwartzman response after their intradermal injection do so by promoting increased intercellular adhesion molecule 1 (ICAM-1) expression on the vascular endothelium. Activation of complement then induces CD11/CD18 expression on circulating leukocytes thus producing an intravascular CD11/CD18-ICAM-1 (leukocyte-endothelium) adhesion event. Inhibition of intravascular leukocyte-leukocyte aggregation with mAb against CD11b (Mac-1) showed partial inhibition of hemorrhage, while mAb against CD11a (LFA-1) showed no inhibitory activity. This type of cytokine-primed, neutrophil-dependent vascular damage may be a model of human vasculitic processes where microvascular damage is produced in the absence of immune-complex deposition.</abstract><cop>United States</cop><pmid>1345915</pmid><doi>10.1172/JCI115570</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Antibodies, Monoclonal - therapeutic use Antigens, CD - immunology Bacterial Toxins - pharmacology Blood Vessels - drug effects Blood Vessels - pathology Cell Adhesion - physiology Cell Adhesion Molecules - immunology Cell Adhesion Molecules - metabolism Cell Adhesion Molecules - toxicity Complement Activation Disease Models, Animal Endotoxins Enterotoxins - pharmacology Female Hemorrhage Integrins - metabolism Intercellular Adhesion Molecule-1 Leukocytes - metabolism Models, Biological Purpura, Schoenlein-Henoch - chemically induced Purpura, Schoenlein-Henoch - metabolism Purpura, Schoenlein-Henoch - therapy Rabbits Skin - drug effects Skin - pathology Zymosan - pharmacology |
title | Interactions of leukocyte integrins with intercellular adhesion molecule 1 in the production of inflammatory vascular injury in vivo. The Shwartzman reaction revisited |
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