Altered Neutrophil Trafficking During Sepsis
In sepsis, dysregulation of the inflammatory system is well known, as reflected in excessive inflammatory mediator production, complement activation, and appearance of defects in phagocytic cells. In the current study sepsis was induced in rats by cecal ligation/puncture. Early in sepsis the beta(1)...
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| Veröffentlicht in: | The Journal of immunology (1950) 2002-07, Vol.169 (1), p.307-314 |
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| container_title | The Journal of immunology (1950) |
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| creator | Guo, Ren-Feng Riedemann, Niels C Laudes, Ines J Sarma, Vidya J Kunkel, Robin G Dilley, Kari A Paulauskis, Joseph D Ward, Peter A |
| description | In sepsis, dysregulation of the inflammatory system is well known, as reflected in excessive inflammatory mediator production, complement activation, and appearance of defects in phagocytic cells. In the current study sepsis was induced in rats by cecal ligation/puncture. Early in sepsis the beta(1) and beta(2) integrin content on blood neutrophils increased in a nontranscriptional manner, and the increase in beta(2), but not beta(1), integrin content was C5a dependent. Similar changes could be induced in vitro on blood neutrophils following contact with phorbol ester or C5a. Direct injury of lungs of normal rats induced by deposition of IgG immune complexes (IgG-IC) caused 5-fold increases in the myeloperoxidase content that was beta(2), but not beta(1), dependent. In contrast, in cecal ligation/puncture lungs myeloperoxidase increased 10-fold after IgG immune complex deposition and was both beta(1) and beta(2) integrin dependent. These data suggest that sepsis causes enhanced neutrophil trafficking into the lung via mechanisms that are not engaged in the nonseptic state. |
| doi_str_mv | 10.4049/jimmunol.169.1.307 |
| format | Article |
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In the current study sepsis was induced in rats by cecal ligation/puncture. Early in sepsis the beta(1) and beta(2) integrin content on blood neutrophils increased in a nontranscriptional manner, and the increase in beta(2), but not beta(1), integrin content was C5a dependent. Similar changes could be induced in vitro on blood neutrophils following contact with phorbol ester or C5a. Direct injury of lungs of normal rats induced by deposition of IgG immune complexes (IgG-IC) caused 5-fold increases in the myeloperoxidase content that was beta(2), but not beta(1), dependent. In contrast, in cecal ligation/puncture lungs myeloperoxidase increased 10-fold after IgG immune complex deposition and was both beta(1) and beta(2) integrin dependent. These data suggest that sepsis causes enhanced neutrophil trafficking into the lung via mechanisms that are not engaged in the nonseptic state.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.169.1.307</identifier><identifier>PMID: 12077259</identifier><language>eng</language><publisher>United States: Am Assoc Immnol</publisher><subject>Animals ; Bronchoalveolar Lavage Fluid - chemistry ; Bronchoalveolar Lavage Fluid - cytology ; CD18 Antigens - biosynthesis ; CD18 Antigens - blood ; CD18 Antigens - immunology ; Complement C5a - antagonists & inhibitors ; Complement C5a - immunology ; Complement C5a - pharmacology ; Disease Models, Animal ; Fibronectins - metabolism ; Flow Cytometry ; Immunoglobulin G - administration & dosage ; Infusions, Intravenous ; Integrin beta1 - biosynthesis ; Integrin beta1 - blood ; Integrin beta1 - immunology ; Ligation ; Lung - enzymology ; Lung - pathology ; Male ; Neutrophil Infiltration - drug effects ; Neutrophil Infiltration - immunology ; Neutrophils - drug effects ; Neutrophils - immunology ; Neutrophils - metabolism ; Neutrophils - pathology ; Peroxidase - metabolism ; Punctures ; Rats ; Rats, Long-Evans ; Sepsis - blood ; Sepsis - enzymology ; Sepsis - immunology ; Sepsis - pathology ; Tetradecanoylphorbol Acetate - pharmacology</subject><ispartof>The Journal of immunology (1950), 2002-07, Vol.169 (1), p.307-314</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-e3e3fffcdad26c12ab09c3cffe3ca131585811edbfa62de56e6d5db1b8ff4683</citedby><cites>FETCH-LOGICAL-c471t-e3e3fffcdad26c12ab09c3cffe3ca131585811edbfa62de56e6d5db1b8ff4683</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12077259$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Ren-Feng</creatorcontrib><creatorcontrib>Riedemann, Niels C</creatorcontrib><creatorcontrib>Laudes, Ines J</creatorcontrib><creatorcontrib>Sarma, Vidya J</creatorcontrib><creatorcontrib>Kunkel, Robin G</creatorcontrib><creatorcontrib>Dilley, Kari A</creatorcontrib><creatorcontrib>Paulauskis, Joseph D</creatorcontrib><creatorcontrib>Ward, Peter A</creatorcontrib><title>Altered Neutrophil Trafficking During Sepsis</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>In sepsis, dysregulation of the inflammatory system is well known, as reflected in excessive inflammatory mediator production, complement activation, and appearance of defects in phagocytic cells. 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These data suggest that sepsis causes enhanced neutrophil trafficking into the lung via mechanisms that are not engaged in the nonseptic state.</description><subject>Animals</subject><subject>Bronchoalveolar Lavage Fluid - chemistry</subject><subject>Bronchoalveolar Lavage Fluid - cytology</subject><subject>CD18 Antigens - biosynthesis</subject><subject>CD18 Antigens - blood</subject><subject>CD18 Antigens - immunology</subject><subject>Complement C5a - antagonists & inhibitors</subject><subject>Complement C5a - immunology</subject><subject>Complement C5a - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Fibronectins - metabolism</subject><subject>Flow Cytometry</subject><subject>Immunoglobulin G - administration & dosage</subject><subject>Infusions, Intravenous</subject><subject>Integrin beta1 - biosynthesis</subject><subject>Integrin beta1 - blood</subject><subject>Integrin beta1 - immunology</subject><subject>Ligation</subject><subject>Lung - enzymology</subject><subject>Lung - pathology</subject><subject>Male</subject><subject>Neutrophil Infiltration - drug effects</subject><subject>Neutrophil Infiltration - immunology</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - immunology</subject><subject>Neutrophils - metabolism</subject><subject>Neutrophils - pathology</subject><subject>Peroxidase - metabolism</subject><subject>Punctures</subject><subject>Rats</subject><subject>Rats, Long-Evans</subject><subject>Sepsis - blood</subject><subject>Sepsis - enzymology</subject><subject>Sepsis - immunology</subject><subject>Sepsis - pathology</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkD1PwzAURS0EoqXwBxhQJyYS_JzYScaqfEoVDHS3HOe5dXGaYDeK-PekalGnu9x7rnQIuQUapzQtHje2rrtt42IQRQxxQrMzMgbOaSQEFedkTCljEWQiG5GrEDaUUkFZeklGwGiWMV6MycPM7dBjNf3Abuebdm3ddOmVMVZ_2-1q-tT5fXxhG2y4JhdGuYA3x5yQ5cvzcv4WLT5f3-ezRaTTDHYRJpgYY3SlKiY0MFXSQifaGEy0ggR4znMArEqjBKuQCxQVr0ooc2NSkScTcn_Atr756TDsZG2DRufUFpsuSMhTxjJOhyI7FLVvQvBoZOttrfyvBCr3iuS_IjkokiAHRcPo7kjvyhqr0-To5HS_tqt1bz3KUCvnhjrIvu9PpD8zCnKP</recordid><startdate>20020701</startdate><enddate>20020701</enddate><creator>Guo, Ren-Feng</creator><creator>Riedemann, Niels C</creator><creator>Laudes, Ines J</creator><creator>Sarma, Vidya J</creator><creator>Kunkel, Robin G</creator><creator>Dilley, Kari A</creator><creator>Paulauskis, Joseph D</creator><creator>Ward, Peter A</creator><general>Am Assoc Immnol</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>7T5</scope><scope>H94</scope></search><sort><creationdate>20020701</creationdate><title>Altered Neutrophil Trafficking During Sepsis</title><author>Guo, Ren-Feng ; 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In the current study sepsis was induced in rats by cecal ligation/puncture. Early in sepsis the beta(1) and beta(2) integrin content on blood neutrophils increased in a nontranscriptional manner, and the increase in beta(2), but not beta(1), integrin content was C5a dependent. Similar changes could be induced in vitro on blood neutrophils following contact with phorbol ester or C5a. Direct injury of lungs of normal rats induced by deposition of IgG immune complexes (IgG-IC) caused 5-fold increases in the myeloperoxidase content that was beta(2), but not beta(1), dependent. In contrast, in cecal ligation/puncture lungs myeloperoxidase increased 10-fold after IgG immune complex deposition and was both beta(1) and beta(2) integrin dependent. 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| subjects | Animals Bronchoalveolar Lavage Fluid - chemistry Bronchoalveolar Lavage Fluid - cytology CD18 Antigens - biosynthesis CD18 Antigens - blood CD18 Antigens - immunology Complement C5a - antagonists & inhibitors Complement C5a - immunology Complement C5a - pharmacology Disease Models, Animal Fibronectins - metabolism Flow Cytometry Immunoglobulin G - administration & dosage Infusions, Intravenous Integrin beta1 - biosynthesis Integrin beta1 - blood Integrin beta1 - immunology Ligation Lung - enzymology Lung - pathology Male Neutrophil Infiltration - drug effects Neutrophil Infiltration - immunology Neutrophils - drug effects Neutrophils - immunology Neutrophils - metabolism Neutrophils - pathology Peroxidase - metabolism Punctures Rats Rats, Long-Evans Sepsis - blood Sepsis - enzymology Sepsis - immunology Sepsis - pathology Tetradecanoylphorbol Acetate - pharmacology |
| title | Altered Neutrophil Trafficking During Sepsis |
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