Induction of the CD23/nitric oxide pathway in endothelial cells downregulates ICAM‐1 expression and decreases cytoadherence of Plasmodium falciparum‐infected erythrocytes
Summary Cytoadherence of parasitized red blood cells (PRBCs) to postcapillary venules and cytokine production are clearly involved in the pathogenesis of cerebral malaria. Nitric oxide and TNF‐α have been proposed as major effector molecules both in protective and physiopathological processes during...
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| Veröffentlicht in: | Cellular microbiology 2004-09, Vol.6 (9), p.839-848 |
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| creator | Pino, Paco Vouldoukis, Ioannis Dugas, Nathalie Conti, Marc Nitcheu, Josiane Traore, Boubacar Danis, Martin Dugas, Bernard Mazier, Dominique |
| description | Summary
Cytoadherence of parasitized red blood cells (PRBCs) to postcapillary venules and cytokine production are clearly involved in the pathogenesis of cerebral malaria. Nitric oxide and TNF‐α have been proposed as major effector molecules both in protective and physiopathological processes during malaria infections. Nitric oxide production has been shown to be induced by engagement of CD23 antigen. This study aimed to investigate the potential role of the CD23/nitric oxide pathway in the control of the cytoadherence of PRBCs on human endothelial cells. We demonstrate that normal human lung endothelial cells (HLECs) are able to express the low affinity receptor for IgE (Fc∈RII/CD23), following cell incubation with interleukin 4 or PRBCs. Ligation of the CD23 antigen by a specific anti‐CD23 monoclonal antibody at the cell surface of HLECs was found to induce iNOS mRNA and protein expression, NO release and P. falciparum killing. In addition, the specific CD23‐engagement on these cells also induced a significant decrease in ICAM‐1 expression, an adhesion molecule implicated in PRBCs cytoadherence. These data not only described for the first time the expression of a CD23 antigen at the cell surface of endothelial cells but also suggest a possible new regulatory mechanisms via the CD23/NO pathway during malaria infection. |
| doi_str_mv | 10.1111/j.1462-5822.2004.00406.x |
| format | Article |
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Cytoadherence of parasitized red blood cells (PRBCs) to postcapillary venules and cytokine production are clearly involved in the pathogenesis of cerebral malaria. Nitric oxide and TNF‐α have been proposed as major effector molecules both in protective and physiopathological processes during malaria infections. Nitric oxide production has been shown to be induced by engagement of CD23 antigen. This study aimed to investigate the potential role of the CD23/nitric oxide pathway in the control of the cytoadherence of PRBCs on human endothelial cells. We demonstrate that normal human lung endothelial cells (HLECs) are able to express the low affinity receptor for IgE (Fc∈RII/CD23), following cell incubation with interleukin 4 or PRBCs. Ligation of the CD23 antigen by a specific anti‐CD23 monoclonal antibody at the cell surface of HLECs was found to induce iNOS mRNA and protein expression, NO release and P. falciparum killing. In addition, the specific CD23‐engagement on these cells also induced a significant decrease in ICAM‐1 expression, an adhesion molecule implicated in PRBCs cytoadherence. These data not only described for the first time the expression of a CD23 antigen at the cell surface of endothelial cells but also suggest a possible new regulatory mechanisms via the CD23/NO pathway during malaria infection.</description><identifier>ISSN: 1462-5814</identifier><identifier>EISSN: 1462-5822</identifier><identifier>DOI: 10.1111/j.1462-5822.2004.00406.x</identifier><identifier>PMID: 15272865</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Animals ; Antimalarials - pharmacology ; Blotting, Northern ; Blotting, Western ; Cell Adhesion ; Cell Culture Techniques ; Cell Line ; Endothelial Cells - metabolism ; Erythrocytes - parasitology ; Gene Expression Regulation ; Humans ; Intercellular Adhesion Molecule-1 - genetics ; Intercellular Adhesion Molecule-1 - metabolism ; Nitric Oxide - metabolism ; Nitric Oxide - pharmacology ; Nitric Oxide Synthase - biosynthesis ; Nitric Oxide Synthase - genetics ; Nitric Oxide Synthase Type II ; Plasmodium falciparum ; Plasmodium falciparum - physiology ; Receptors, IgE - genetics ; Receptors, IgE - metabolism ; RNA, Messenger - analysis</subject><ispartof>Cellular microbiology, 2004-09, Vol.6 (9), p.839-848</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4126-1c78d7884ab6b52c7d336977a490ab9702fe3682d0f662b6197aa4b9ef963e5e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1462-5822.2004.00406.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1462-5822.2004.00406.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15272865$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pino, Paco</creatorcontrib><creatorcontrib>Vouldoukis, Ioannis</creatorcontrib><creatorcontrib>Dugas, Nathalie</creatorcontrib><creatorcontrib>Conti, Marc</creatorcontrib><creatorcontrib>Nitcheu, Josiane</creatorcontrib><creatorcontrib>Traore, Boubacar</creatorcontrib><creatorcontrib>Danis, Martin</creatorcontrib><creatorcontrib>Dugas, Bernard</creatorcontrib><creatorcontrib>Mazier, Dominique</creatorcontrib><title>Induction of the CD23/nitric oxide pathway in endothelial cells downregulates ICAM‐1 expression and decreases cytoadherence of Plasmodium falciparum‐infected erythrocytes</title><title>Cellular microbiology</title><addtitle>Cell Microbiol</addtitle><description>Summary
Cytoadherence of parasitized red blood cells (PRBCs) to postcapillary venules and cytokine production are clearly involved in the pathogenesis of cerebral malaria. Nitric oxide and TNF‐α have been proposed as major effector molecules both in protective and physiopathological processes during malaria infections. Nitric oxide production has been shown to be induced by engagement of CD23 antigen. This study aimed to investigate the potential role of the CD23/nitric oxide pathway in the control of the cytoadherence of PRBCs on human endothelial cells. We demonstrate that normal human lung endothelial cells (HLECs) are able to express the low affinity receptor for IgE (Fc∈RII/CD23), following cell incubation with interleukin 4 or PRBCs. Ligation of the CD23 antigen by a specific anti‐CD23 monoclonal antibody at the cell surface of HLECs was found to induce iNOS mRNA and protein expression, NO release and P. falciparum killing. In addition, the specific CD23‐engagement on these cells also induced a significant decrease in ICAM‐1 expression, an adhesion molecule implicated in PRBCs cytoadherence. These data not only described for the first time the expression of a CD23 antigen at the cell surface of endothelial cells but also suggest a possible new regulatory mechanisms via the CD23/NO pathway during malaria infection.</description><subject>Animals</subject><subject>Antimalarials - pharmacology</subject><subject>Blotting, Northern</subject><subject>Blotting, Western</subject><subject>Cell Adhesion</subject><subject>Cell Culture Techniques</subject><subject>Cell Line</subject><subject>Endothelial Cells - metabolism</subject><subject>Erythrocytes - parasitology</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Intercellular Adhesion Molecule-1 - genetics</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide - pharmacology</subject><subject>Nitric Oxide Synthase - biosynthesis</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Plasmodium falciparum</subject><subject>Plasmodium falciparum - physiology</subject><subject>Receptors, IgE - genetics</subject><subject>Receptors, IgE - metabolism</subject><subject>RNA, Messenger - analysis</subject><issn>1462-5814</issn><issn>1462-5822</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFu1DAQhi0EoqXwCsgnbpvaTmInEhe0lLJSKzjA2XLsCetVYgfb0W5uPAJPwkP1SXBoKUcsWR5pPv-j0YcQpqSg-VweClpxtqkbxgpGSFXkS3hxeoLOHxtPH2tanaEXMR4IoVxQ-hyd0ZoJ1vD6HP3aOTPrZL3DvsdpD3j7npWXzqZgNfYnawBPKu2PasHWYXDGZ2iwasAahiFi448uwLd5UAki3m3f3d79-EkxnKYAMa65yhlsQAdQMRN6SV6ZPQRwGtaZnwcVR2_sPOJeDdpOKsxjzrCuB53AYAhL2gefP0J8iZ5lKMKrh_cCff1w9WX7cXPz6TrPvtnoijK-oVo0RjRNpTre1UwLU5a8FUJVLVFdKwjroeQNM6TnnHWctkKpqmuhb3kJNZQX6M197hT89xlikqON68LKgZ-j5FxUpGnq_4JUCMoELzP4-gGcuxGMnIIdVVjkXxUZeHsPHO0Ay78-katyeZCrTbmalaty-Ue5PMnt7S4X5W-FJ6Qf</recordid><startdate>200409</startdate><enddate>200409</enddate><creator>Pino, Paco</creator><creator>Vouldoukis, Ioannis</creator><creator>Dugas, Nathalie</creator><creator>Conti, Marc</creator><creator>Nitcheu, Josiane</creator><creator>Traore, Boubacar</creator><creator>Danis, Martin</creator><creator>Dugas, Bernard</creator><creator>Mazier, Dominique</creator><general>Blackwell Science Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>M7N</scope><scope>7X8</scope></search><sort><creationdate>200409</creationdate><title>Induction of the CD23/nitric oxide pathway in endothelial cells downregulates ICAM‐1 expression and decreases cytoadherence of Plasmodium falciparum‐infected erythrocytes</title><author>Pino, Paco ; Vouldoukis, Ioannis ; Dugas, Nathalie ; Conti, Marc ; Nitcheu, Josiane ; Traore, Boubacar ; Danis, Martin ; Dugas, Bernard ; Mazier, Dominique</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4126-1c78d7884ab6b52c7d336977a490ab9702fe3682d0f662b6197aa4b9ef963e5e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Antimalarials - pharmacology</topic><topic>Blotting, Northern</topic><topic>Blotting, Western</topic><topic>Cell Adhesion</topic><topic>Cell Culture Techniques</topic><topic>Cell Line</topic><topic>Endothelial Cells - metabolism</topic><topic>Erythrocytes - parasitology</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Intercellular Adhesion Molecule-1 - genetics</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide - pharmacology</topic><topic>Nitric Oxide Synthase - biosynthesis</topic><topic>Nitric Oxide Synthase - genetics</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Plasmodium falciparum</topic><topic>Plasmodium falciparum - physiology</topic><topic>Receptors, IgE - genetics</topic><topic>Receptors, IgE - metabolism</topic><topic>RNA, Messenger - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pino, Paco</creatorcontrib><creatorcontrib>Vouldoukis, Ioannis</creatorcontrib><creatorcontrib>Dugas, Nathalie</creatorcontrib><creatorcontrib>Conti, Marc</creatorcontrib><creatorcontrib>Nitcheu, Josiane</creatorcontrib><creatorcontrib>Traore, Boubacar</creatorcontrib><creatorcontrib>Danis, Martin</creatorcontrib><creatorcontrib>Dugas, Bernard</creatorcontrib><creatorcontrib>Mazier, Dominique</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><jtitle>Cellular microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pino, Paco</au><au>Vouldoukis, Ioannis</au><au>Dugas, Nathalie</au><au>Conti, Marc</au><au>Nitcheu, Josiane</au><au>Traore, Boubacar</au><au>Danis, Martin</au><au>Dugas, Bernard</au><au>Mazier, Dominique</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induction of the CD23/nitric oxide pathway in endothelial cells downregulates ICAM‐1 expression and decreases cytoadherence of Plasmodium falciparum‐infected erythrocytes</atitle><jtitle>Cellular microbiology</jtitle><addtitle>Cell Microbiol</addtitle><date>2004-09</date><risdate>2004</risdate><volume>6</volume><issue>9</issue><spage>839</spage><epage>848</epage><pages>839-848</pages><issn>1462-5814</issn><eissn>1462-5822</eissn><abstract>Summary
Cytoadherence of parasitized red blood cells (PRBCs) to postcapillary venules and cytokine production are clearly involved in the pathogenesis of cerebral malaria. Nitric oxide and TNF‐α have been proposed as major effector molecules both in protective and physiopathological processes during malaria infections. Nitric oxide production has been shown to be induced by engagement of CD23 antigen. This study aimed to investigate the potential role of the CD23/nitric oxide pathway in the control of the cytoadherence of PRBCs on human endothelial cells. We demonstrate that normal human lung endothelial cells (HLECs) are able to express the low affinity receptor for IgE (Fc∈RII/CD23), following cell incubation with interleukin 4 or PRBCs. Ligation of the CD23 antigen by a specific anti‐CD23 monoclonal antibody at the cell surface of HLECs was found to induce iNOS mRNA and protein expression, NO release and P. falciparum killing. In addition, the specific CD23‐engagement on these cells also induced a significant decrease in ICAM‐1 expression, an adhesion molecule implicated in PRBCs cytoadherence. These data not only described for the first time the expression of a CD23 antigen at the cell surface of endothelial cells but also suggest a possible new regulatory mechanisms via the CD23/NO pathway during malaria infection.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>15272865</pmid><doi>10.1111/j.1462-5822.2004.00406.x</doi><tpages>10</tpages></addata></record> |
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| ispartof | Cellular microbiology, 2004-09, Vol.6 (9), p.839-848 |
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| source | Wiley Free Content; MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Antimalarials - pharmacology Blotting, Northern Blotting, Western Cell Adhesion Cell Culture Techniques Cell Line Endothelial Cells - metabolism Erythrocytes - parasitology Gene Expression Regulation Humans Intercellular Adhesion Molecule-1 - genetics Intercellular Adhesion Molecule-1 - metabolism Nitric Oxide - metabolism Nitric Oxide - pharmacology Nitric Oxide Synthase - biosynthesis Nitric Oxide Synthase - genetics Nitric Oxide Synthase Type II Plasmodium falciparum Plasmodium falciparum - physiology Receptors, IgE - genetics Receptors, IgE - metabolism RNA, Messenger - analysis |
| title | Induction of the CD23/nitric oxide pathway in endothelial cells downregulates ICAM‐1 expression and decreases cytoadherence of Plasmodium falciparum‐infected erythrocytes |
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