Induction of type-IIA secretory phospholipase A2 in animal models of acute lung injury
The aim of this study was to evaluate the presence of type-II secretory phospholipase A2 (sPLA2-IIA) in alveolar space and its possible role in the destruction of surfactant in three rat models of acute lung injury. Alveolar instillation of either lipopolysaccaride or live Pseudomonas aeruginosa res...
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| Veröffentlicht in: | The European respiratory journal 2003-06, Vol.21 (6), p.1040-1045 |
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| creator | Attalah, H.L Wu, Y Alaoui-El-Azher, M Thouron, F Koumanov, K Wolf, C Brochard, L Harf, A Delclaux, C Touqui, L |
| description | The aim of this study was to evaluate the presence of type-II secretory phospholipase A2 (sPLA2-IIA) in alveolar space and its possible role in the destruction of surfactant in three rat models of acute lung injury. Alveolar instillation of either lipopolysaccaride or live Pseudomonas aeruginosa resulted in a significant increase in lung oedema and in a decrease in static compliance of the respiratory system together with alveolar-neutrophil influx as compared with healthy control rats. The upregulation of messenger ribonucleic acid and sPLA2-IIA by the lung was evident. This was associated with surfactant degradation and a decrease in large:small ratio of surfactant aggregates in bacteria-instilled rats. A negative correlation between compliance and sPLA2-IIA activity in bronchoalveolar lavage fluid was shown. By contrast, during alpha naphthylthiourea-induced injury, neither alveolar-neutrophil influx nor increase in sPLA2-IIA activity was observed. Additional experiments in rats treated with a specific inhibitor of type-II secretory phospholipase A2 activity (3 acetamine-1-benzyl-2 ethylindolyl-5 oxy; propane phosphonic acid (LY311727)) demonstrated no improvement in physiological parameters despite a biochemical effect, suggesting that its activity is only one of the multiple factors involved in the pathophysiology of lung injury. |
| doi_str_mv | 10.1183/09031936.03.00093002 |
| format | Article |
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Alveolar instillation of either lipopolysaccaride or live Pseudomonas aeruginosa resulted in a significant increase in lung oedema and in a decrease in static compliance of the respiratory system together with alveolar-neutrophil influx as compared with healthy control rats. The upregulation of messenger ribonucleic acid and sPLA2-IIA by the lung was evident. This was associated with surfactant degradation and a decrease in large:small ratio of surfactant aggregates in bacteria-instilled rats. A negative correlation between compliance and sPLA2-IIA activity in bronchoalveolar lavage fluid was shown. By contrast, during alpha naphthylthiourea-induced injury, neither alveolar-neutrophil influx nor increase in sPLA2-IIA activity was observed. Additional experiments in rats treated with a specific inhibitor of type-II secretory phospholipase A2 activity (3 acetamine-1-benzyl-2 ethylindolyl-5 oxy; propane phosphonic acid (LY311727)) demonstrated no improvement in physiological parameters despite a biochemical effect, suggesting that its activity is only one of the multiple factors involved in the pathophysiology of lung injury.</description><identifier>ISSN: 0903-1936</identifier><identifier>EISSN: 1399-3003</identifier><identifier>DOI: 10.1183/09031936.03.00093002</identifier><identifier>PMID: 12797501</identifier><language>eng</language><publisher>Leeds: Eur Respiratory Soc</publisher><subject>Animals ; Biological and medical sciences ; Bronchoalveolar Lavage Fluid - chemistry ; Disease Models, Animal ; Group II Phospholipases A2 ; Human health and pathology ; Life Sciences ; Lung Compliance - physiology ; Male ; Medical sciences ; Phospholipases A - analysis ; Phospholipases A - physiology ; Phospholipases A2 ; Pneumology ; Pneumonia - complications ; Pneumonia - physiopathology ; Pulmonary Alveoli - chemistry ; Pulmonary Alveoli - physiopathology ; Pulmonary Edema - complications ; Pulmonary Edema - physiopathology ; Pulmonary Surfactants - chemistry ; Pulmonology and respiratory tract ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult - etiology ; Respiratory Distress Syndrome, Adult - physiopathology ; Respiratory system : syndromes and miscellaneous diseases ; Severity of Illness Index</subject><ispartof>The European respiratory journal, 2003-06, Vol.21 (6), p.1040-1045</ispartof><rights>2003 INIST-CNRS</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-3a76f446c9a846c6dd1baaba24e081b287ce2eb3a850ac39180f6f114999123b3</citedby><cites>FETCH-LOGICAL-c448t-3a76f446c9a846c6dd1baaba24e081b287ce2eb3a850ac39180f6f114999123b3</cites><orcidid>0000-0003-0050-8480 ; 0000-0003-2786-0812 ; 0000-0002-4569-016X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14788257$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12797501$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://pasteur.hal.science/pasteur-02863076$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Attalah, H.L</creatorcontrib><creatorcontrib>Wu, Y</creatorcontrib><creatorcontrib>Alaoui-El-Azher, M</creatorcontrib><creatorcontrib>Thouron, F</creatorcontrib><creatorcontrib>Koumanov, K</creatorcontrib><creatorcontrib>Wolf, C</creatorcontrib><creatorcontrib>Brochard, L</creatorcontrib><creatorcontrib>Harf, A</creatorcontrib><creatorcontrib>Delclaux, C</creatorcontrib><creatorcontrib>Touqui, L</creatorcontrib><title>Induction of type-IIA secretory phospholipase A2 in animal models of acute lung injury</title><title>The European respiratory journal</title><addtitle>Eur Respir J</addtitle><description>The aim of this study was to evaluate the presence of type-II secretory phospholipase A2 (sPLA2-IIA) in alveolar space and its possible role in the destruction of surfactant in three rat models of acute lung injury. Alveolar instillation of either lipopolysaccaride or live Pseudomonas aeruginosa resulted in a significant increase in lung oedema and in a decrease in static compliance of the respiratory system together with alveolar-neutrophil influx as compared with healthy control rats. The upregulation of messenger ribonucleic acid and sPLA2-IIA by the lung was evident. This was associated with surfactant degradation and a decrease in large:small ratio of surfactant aggregates in bacteria-instilled rats. A negative correlation between compliance and sPLA2-IIA activity in bronchoalveolar lavage fluid was shown. By contrast, during alpha naphthylthiourea-induced injury, neither alveolar-neutrophil influx nor increase in sPLA2-IIA activity was observed. Additional experiments in rats treated with a specific inhibitor of type-II secretory phospholipase A2 activity (3 acetamine-1-benzyl-2 ethylindolyl-5 oxy; propane phosphonic acid (LY311727)) demonstrated no improvement in physiological parameters despite a biochemical effect, suggesting that its activity is only one of the multiple factors involved in the pathophysiology of lung injury.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bronchoalveolar Lavage Fluid - chemistry</subject><subject>Disease Models, Animal</subject><subject>Group II Phospholipases A2</subject><subject>Human health and pathology</subject><subject>Life Sciences</subject><subject>Lung Compliance - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Phospholipases A - analysis</subject><subject>Phospholipases A - physiology</subject><subject>Phospholipases A2</subject><subject>Pneumology</subject><subject>Pneumonia - complications</subject><subject>Pneumonia - physiopathology</subject><subject>Pulmonary Alveoli - chemistry</subject><subject>Pulmonary Alveoli - physiopathology</subject><subject>Pulmonary Edema - complications</subject><subject>Pulmonary Edema - physiopathology</subject><subject>Pulmonary Surfactants - chemistry</subject><subject>Pulmonology and respiratory tract</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Respiratory Distress Syndrome, Adult - etiology</subject><subject>Respiratory Distress Syndrome, Adult - physiopathology</subject><subject>Respiratory system : syndromes and miscellaneous diseases</subject><subject>Severity of Illness Index</subject><issn>0903-1936</issn><issn>1399-3003</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEGP0zAQhS0EYsvCP0AoF7ilzNiuYx-r1cJWqsQFuFqO42xduXGwE1D_Pa4a6GE8I_l7T0-PkPcIa0TJPoMChoqJNbA1ACgGQF-QFTKl6nKzl2R1QeoLc0fe5HwEQMEZviZ3SBvVbABX5Odu6GY7-ThUsa-m8-jq3W5bZWeTm2I6V-Mh5jLBjya7aksrP1Rm8CcTqlPsXMgXnbHz5KowD8_l-zin81vyqjchu3fLvic_vjx-f3iq99--7h62-9pyLqeamUb0nAurjCyv6DpsjWkN5Q4ktlQ21lHXMiM3YCxTKKEXPSJXSiFlLbsn9dX3YIIeU4mVzjoar5-2e10ST25OGqgUDBrxGwv_6cqPKf6aXZ70yWfrQjCDi3PWDWMbRrkoIL-CNsWck-v_uyPoS__6X_8ayr30X2QfFv-5PbnuJloKL8DHBTDZmtAnM1ifbxxvpKSb5hb04J8Pf3xyOpfKQ7FF7dKRohYlCQf2FwlzmRY</recordid><startdate>20030601</startdate><enddate>20030601</enddate><creator>Attalah, H.L</creator><creator>Wu, Y</creator><creator>Alaoui-El-Azher, M</creator><creator>Thouron, F</creator><creator>Koumanov, K</creator><creator>Wolf, C</creator><creator>Brochard, L</creator><creator>Harf, A</creator><creator>Delclaux, C</creator><creator>Touqui, L</creator><general>Eur Respiratory Soc</general><general>Maney</general><general>European Respiratory Society</general><scope>IQODW</scope><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><scope>1XC</scope><orcidid>https://orcid.org/0000-0003-0050-8480</orcidid><orcidid>https://orcid.org/0000-0003-2786-0812</orcidid><orcidid>https://orcid.org/0000-0002-4569-016X</orcidid></search><sort><creationdate>20030601</creationdate><title>Induction of type-IIA secretory phospholipase A2 in animal models of acute lung injury</title><author>Attalah, H.L ; Wu, Y ; Alaoui-El-Azher, M ; Thouron, F ; Koumanov, K ; Wolf, C ; Brochard, L ; Harf, A ; Delclaux, C ; Touqui, L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-3a76f446c9a846c6dd1baaba24e081b287ce2eb3a850ac39180f6f114999123b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bronchoalveolar Lavage Fluid - chemistry</topic><topic>Disease Models, Animal</topic><topic>Group II Phospholipases A2</topic><topic>Human health and pathology</topic><topic>Life Sciences</topic><topic>Lung Compliance - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Phospholipases A - analysis</topic><topic>Phospholipases A - physiology</topic><topic>Phospholipases A2</topic><topic>Pneumology</topic><topic>Pneumonia - complications</topic><topic>Pneumonia - physiopathology</topic><topic>Pulmonary Alveoli - chemistry</topic><topic>Pulmonary Alveoli - physiopathology</topic><topic>Pulmonary Edema - complications</topic><topic>Pulmonary Edema - physiopathology</topic><topic>Pulmonary Surfactants - chemistry</topic><topic>Pulmonology and respiratory tract</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Respiratory Distress Syndrome, Adult - etiology</topic><topic>Respiratory Distress Syndrome, Adult - physiopathology</topic><topic>Respiratory system : syndromes and miscellaneous diseases</topic><topic>Severity of Illness Index</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Attalah, H.L</creatorcontrib><creatorcontrib>Wu, Y</creatorcontrib><creatorcontrib>Alaoui-El-Azher, M</creatorcontrib><creatorcontrib>Thouron, F</creatorcontrib><creatorcontrib>Koumanov, K</creatorcontrib><creatorcontrib>Wolf, C</creatorcontrib><creatorcontrib>Brochard, L</creatorcontrib><creatorcontrib>Harf, A</creatorcontrib><creatorcontrib>Delclaux, C</creatorcontrib><creatorcontrib>Touqui, L</creatorcontrib><collection>Pascal-Francis</collection><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><collection>Hyper Article en Ligne (HAL)</collection><jtitle>The European respiratory journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Attalah, H.L</au><au>Wu, Y</au><au>Alaoui-El-Azher, M</au><au>Thouron, F</au><au>Koumanov, K</au><au>Wolf, C</au><au>Brochard, L</au><au>Harf, A</au><au>Delclaux, C</au><au>Touqui, L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induction of type-IIA secretory phospholipase A2 in animal models of acute lung injury</atitle><jtitle>The European respiratory journal</jtitle><addtitle>Eur Respir J</addtitle><date>2003-06-01</date><risdate>2003</risdate><volume>21</volume><issue>6</issue><spage>1040</spage><epage>1045</epage><pages>1040-1045</pages><issn>0903-1936</issn><eissn>1399-3003</eissn><abstract>The aim of this study was to evaluate the presence of type-II secretory phospholipase A2 (sPLA2-IIA) in alveolar space and its possible role in the destruction of surfactant in three rat models of acute lung injury. Alveolar instillation of either lipopolysaccaride or live Pseudomonas aeruginosa resulted in a significant increase in lung oedema and in a decrease in static compliance of the respiratory system together with alveolar-neutrophil influx as compared with healthy control rats. The upregulation of messenger ribonucleic acid and sPLA2-IIA by the lung was evident. This was associated with surfactant degradation and a decrease in large:small ratio of surfactant aggregates in bacteria-instilled rats. A negative correlation between compliance and sPLA2-IIA activity in bronchoalveolar lavage fluid was shown. By contrast, during alpha naphthylthiourea-induced injury, neither alveolar-neutrophil influx nor increase in sPLA2-IIA activity was observed. Additional experiments in rats treated with a specific inhibitor of type-II secretory phospholipase A2 activity (3 acetamine-1-benzyl-2 ethylindolyl-5 oxy; propane phosphonic acid (LY311727)) demonstrated no improvement in physiological parameters despite a biochemical effect, suggesting that its activity is only one of the multiple factors involved in the pathophysiology of lung injury.</abstract><cop>Leeds</cop><pub>Eur Respiratory Soc</pub><pmid>12797501</pmid><doi>10.1183/09031936.03.00093002</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0003-0050-8480</orcidid><orcidid>https://orcid.org/0000-0003-2786-0812</orcidid><orcidid>https://orcid.org/0000-0002-4569-016X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Bronchoalveolar Lavage Fluid - chemistry Disease Models, Animal Group II Phospholipases A2 Human health and pathology Life Sciences Lung Compliance - physiology Male Medical sciences Phospholipases A - analysis Phospholipases A - physiology Phospholipases A2 Pneumology Pneumonia - complications Pneumonia - physiopathology Pulmonary Alveoli - chemistry Pulmonary Alveoli - physiopathology Pulmonary Edema - complications Pulmonary Edema - physiopathology Pulmonary Surfactants - chemistry Pulmonology and respiratory tract Rats Rats, Sprague-Dawley Respiratory Distress Syndrome, Adult - etiology Respiratory Distress Syndrome, Adult - physiopathology Respiratory system : syndromes and miscellaneous diseases Severity of Illness Index |
| title | Induction of type-IIA secretory phospholipase A2 in animal models of acute lung injury |
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