The apoptosis of neutrophils is accelerated in respiratory syncytial virus (RSV)‐induced bronchiolitis
Neutrophils are the predominant inflammatory cell in the lung tissues and airways in RSV infection, and can augment the epithelial cell damage induced by RSV. Neutrophil apoptosis has been suggested to be a mechanism to reduce the potential for tissue injury. The apoptosis of neutrophils from nasoph...
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Veröffentlicht in: | Clinical and experimental immunology 1998-10, Vol.114 (1), p.49-54 |
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description | Neutrophils are the predominant inflammatory cell in the lung tissues and airways in RSV infection, and can augment the epithelial cell damage induced by RSV. Neutrophil apoptosis has been suggested to be a mechanism to reduce the potential for tissue injury. The apoptosis of neutrophils from nasopharyngeal aspirates (NPA) (n = 19) and peripheral blood (PB) of infants with RSV bronchiolitis (n = 11) and PB from healthy controls (n = 9) was investigated. Monoclonal antibody against CD95 (Fas) and a binding protein Annexin V were used to determine the apoptosis of neutrophils. The expression of CD11b and CD18 on neutrophils was also detected with flow cytometry. The mean fluorescence intensity (MFI) of CD95 on neutrophils from RSV+ NPA was increased compared with cells from control PB (73.6 ± 7.6 versus 31.5 ± 4.3); the MFI of Annexin V, CD11b and CD18 on neutrophils from RSV+ NPA was up‐regulated compared with cells from both control PB (105.3 ± 18.1 versus 11.8 ± 1.5; 1683 ± 153.3 versus 841.1 ± 72.3; 517 ± 50.5 versus 147 ± 8.7, respectively) and RSV+ PB (105.3 ± 18.1 versus 35.8 ± 4.1; 1683 ± 153.3 versus 818 ± 141.2; 517 ± 50.5 versus 260 ± 25.8, respectively). Furthermore, the percentage of neutrophils expressing Annexin V and the MFI of CD18 on neutrophils from RSV+ PB were increased compared with neutrophils from control PB. In addition, both CD11b (MFI) and CD18 (MFI) correlated with Annexin V (MFI) on neutrophils. We conclude that neutrophil apoptosis in RSV bronchiolitis is accelerated; and CD11b/CD18 may play an important role in RSV infection by influencing neutrophil apoptosis. |
doi_str_mv | 10.1046/j.1365-2249.1998.00681.x |
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K ; LOVEJOY, M ; BOWDEN, J. J ; ALPERS, J. H ; FORSYTH, K. D</creator><creatorcontrib>WANG, S.-Z ; SMITH, P. K ; LOVEJOY, M ; BOWDEN, J. J ; ALPERS, J. H ; FORSYTH, K. D</creatorcontrib><description>Neutrophils are the predominant inflammatory cell in the lung tissues and airways in RSV infection, and can augment the epithelial cell damage induced by RSV. Neutrophil apoptosis has been suggested to be a mechanism to reduce the potential for tissue injury. The apoptosis of neutrophils from nasopharyngeal aspirates (NPA) (n = 19) and peripheral blood (PB) of infants with RSV bronchiolitis (n = 11) and PB from healthy controls (n = 9) was investigated. Monoclonal antibody against CD95 (Fas) and a binding protein Annexin V were used to determine the apoptosis of neutrophils. The expression of CD11b and CD18 on neutrophils was also detected with flow cytometry. The mean fluorescence intensity (MFI) of CD95 on neutrophils from RSV+ NPA was increased compared with cells from control PB (73.6 ± 7.6 versus 31.5 ± 4.3); the MFI of Annexin V, CD11b and CD18 on neutrophils from RSV+ NPA was up‐regulated compared with cells from both control PB (105.3 ± 18.1 versus 11.8 ± 1.5; 1683 ± 153.3 versus 841.1 ± 72.3; 517 ± 50.5 versus 147 ± 8.7, respectively) and RSV+ PB (105.3 ± 18.1 versus 35.8 ± 4.1; 1683 ± 153.3 versus 818 ± 141.2; 517 ± 50.5 versus 260 ± 25.8, respectively). Furthermore, the percentage of neutrophils expressing Annexin V and the MFI of CD18 on neutrophils from RSV+ PB were increased compared with neutrophils from control PB. In addition, both CD11b (MFI) and CD18 (MFI) correlated with Annexin V (MFI) on neutrophils. We conclude that neutrophil apoptosis in RSV bronchiolitis is accelerated; and CD11b/CD18 may play an important role in RSV infection by influencing neutrophil apoptosis.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1046/j.1365-2249.1998.00681.x</identifier><identifier>PMID: 9764602</identifier><identifier>CODEN: CEXIAL</identifier><language>eng</language><publisher>Oxford BSL: Blackwell Science Ltd</publisher><subject>Annexin A5 - biosynthesis ; Apoptosis ; Biological and medical sciences ; bronchiolitis ; Bronchiolitis - immunology ; Bronchiolitis - virology ; CD18 Antigens - biosynthesis ; fas Receptor - biosynthesis ; Human viral diseases ; Humans ; Infant ; Infectious diseases ; Macrophage-1 Antigen - biosynthesis ; Medical sciences ; neutrophil ; Neutrophils - metabolism ; Original ; regulation ; respiratory syncytial virus ; Respiratory Syncytial Virus Infections - immunology ; Respiratory Syncytial Virus, Human ; Viral diseases ; Viral diseases of the respiratory system and ent viral diseases</subject><ispartof>Clinical and experimental immunology, 1998-10, Vol.114 (1), p.49-54</ispartof><rights>Blackwell Science Ltd, Oxford</rights><rights>1998 INIST-CNRS</rights><rights>Copyright Blackwell Scientific Publications Ltd. Oct 1998</rights><rights>1998 Blackwell Science Ltd 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5551-25d2b2ce6f0307a110095ba56f5a347ec5d889241414be031606ba01010c67103</citedby><cites>FETCH-LOGICAL-c5551-25d2b2ce6f0307a110095ba56f5a347ec5d889241414be031606ba01010c67103</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1905089/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1905089/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2397896$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9764602$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WANG, S.-Z</creatorcontrib><creatorcontrib>SMITH, P. K</creatorcontrib><creatorcontrib>LOVEJOY, M</creatorcontrib><creatorcontrib>BOWDEN, J. J</creatorcontrib><creatorcontrib>ALPERS, J. H</creatorcontrib><creatorcontrib>FORSYTH, K. D</creatorcontrib><title>The apoptosis of neutrophils is accelerated in respiratory syncytial virus (RSV)‐induced bronchiolitis</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>Neutrophils are the predominant inflammatory cell in the lung tissues and airways in RSV infection, and can augment the epithelial cell damage induced by RSV. Neutrophil apoptosis has been suggested to be a mechanism to reduce the potential for tissue injury. The apoptosis of neutrophils from nasopharyngeal aspirates (NPA) (n = 19) and peripheral blood (PB) of infants with RSV bronchiolitis (n = 11) and PB from healthy controls (n = 9) was investigated. Monoclonal antibody against CD95 (Fas) and a binding protein Annexin V were used to determine the apoptosis of neutrophils. The expression of CD11b and CD18 on neutrophils was also detected with flow cytometry. The mean fluorescence intensity (MFI) of CD95 on neutrophils from RSV+ NPA was increased compared with cells from control PB (73.6 ± 7.6 versus 31.5 ± 4.3); the MFI of Annexin V, CD11b and CD18 on neutrophils from RSV+ NPA was up‐regulated compared with cells from both control PB (105.3 ± 18.1 versus 11.8 ± 1.5; 1683 ± 153.3 versus 841.1 ± 72.3; 517 ± 50.5 versus 147 ± 8.7, respectively) and RSV+ PB (105.3 ± 18.1 versus 35.8 ± 4.1; 1683 ± 153.3 versus 818 ± 141.2; 517 ± 50.5 versus 260 ± 25.8, respectively). Furthermore, the percentage of neutrophils expressing Annexin V and the MFI of CD18 on neutrophils from RSV+ PB were increased compared with neutrophils from control PB. In addition, both CD11b (MFI) and CD18 (MFI) correlated with Annexin V (MFI) on neutrophils. We conclude that neutrophil apoptosis in RSV bronchiolitis is accelerated; and CD11b/CD18 may play an important role in RSV infection by influencing neutrophil apoptosis.</description><subject>Annexin A5 - biosynthesis</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>bronchiolitis</subject><subject>Bronchiolitis - immunology</subject><subject>Bronchiolitis - virology</subject><subject>CD18 Antigens - biosynthesis</subject><subject>fas Receptor - biosynthesis</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>Infant</subject><subject>Infectious diseases</subject><subject>Macrophage-1 Antigen - biosynthesis</subject><subject>Medical sciences</subject><subject>neutrophil</subject><subject>Neutrophils - metabolism</subject><subject>Original</subject><subject>regulation</subject><subject>respiratory syncytial virus</subject><subject>Respiratory Syncytial Virus Infections - immunology</subject><subject>Respiratory Syncytial Virus, Human</subject><subject>Viral diseases</subject><subject>Viral diseases of the respiratory system and ent viral diseases</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUd2K1DAYDaKs4-ojCEFk0YvWpG3SBmRBht11YUHQ1duQpqnN0Elq0q7bOx_BZ9wn8evOMKg3Si6SL-d8P-c7CGFKUkoK_maT0pyzJMsKkVIhqpQQXtH09gFaHYCHaEUIEYmAjMfoSYwbCDnn2RE6EiUvOMlWqLvuDFaDH0YfbcS-xc5MY_BDZ_uI4UdpbXoT1GgabB0OJg4WIh9mHGen59GqHt_YMEX86uOnL6_vfvy0rpk00Ovgne6s7-1o41P0qFV9NM_29zH6fH52vX6fXH24uFy_u0o0Y4wmGWuyOtOGtyQnpaIUFLBaMd4ylRel0aypKpEVFE5tSE454bUiFI7mJSX5MTrd1R2memsabdwYVC-HYLcqzNIrK_9EnO3kV38jqSCMVAIKnOwLBP9tMnGUWxthB71yxk9Rlrko8yz_N5HyQpTgBhBf_EXc-Ck42AI05RWvQDmQqh1JBx9jMO1hZErk4rncyMVauVgrF8_lvefyFlKf_y75kLg3GfCXe1xFrfo2KKdtPNBAS1mJZcy3O9p325v5v9vL9dklPPJfAzPI7g</recordid><startdate>199810</startdate><enddate>199810</enddate><creator>WANG, S.-Z</creator><creator>SMITH, P. K</creator><creator>LOVEJOY, M</creator><creator>BOWDEN, J. J</creator><creator>ALPERS, J. H</creator><creator>FORSYTH, K. D</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Oxford University Press</general><general>Blackwell Science Inc</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>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>199810</creationdate><title>The apoptosis of neutrophils is accelerated in respiratory syncytial virus (RSV)‐induced bronchiolitis</title><author>WANG, S.-Z ; SMITH, P. K ; LOVEJOY, M ; BOWDEN, J. J ; ALPERS, J. H ; FORSYTH, K. 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K</creatorcontrib><creatorcontrib>LOVEJOY, M</creatorcontrib><creatorcontrib>BOWDEN, J. J</creatorcontrib><creatorcontrib>ALPERS, J. H</creatorcontrib><creatorcontrib>FORSYTH, K. D</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>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WANG, S.-Z</au><au>SMITH, P. K</au><au>LOVEJOY, M</au><au>BOWDEN, J. J</au><au>ALPERS, J. H</au><au>FORSYTH, K. D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The apoptosis of neutrophils is accelerated in respiratory syncytial virus (RSV)‐induced bronchiolitis</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>1998-10</date><risdate>1998</risdate><volume>114</volume><issue>1</issue><spage>49</spage><epage>54</epage><pages>49-54</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><coden>CEXIAL</coden><abstract>Neutrophils are the predominant inflammatory cell in the lung tissues and airways in RSV infection, and can augment the epithelial cell damage induced by RSV. Neutrophil apoptosis has been suggested to be a mechanism to reduce the potential for tissue injury. The apoptosis of neutrophils from nasopharyngeal aspirates (NPA) (n = 19) and peripheral blood (PB) of infants with RSV bronchiolitis (n = 11) and PB from healthy controls (n = 9) was investigated. Monoclonal antibody against CD95 (Fas) and a binding protein Annexin V were used to determine the apoptosis of neutrophils. The expression of CD11b and CD18 on neutrophils was also detected with flow cytometry. The mean fluorescence intensity (MFI) of CD95 on neutrophils from RSV+ NPA was increased compared with cells from control PB (73.6 ± 7.6 versus 31.5 ± 4.3); the MFI of Annexin V, CD11b and CD18 on neutrophils from RSV+ NPA was up‐regulated compared with cells from both control PB (105.3 ± 18.1 versus 11.8 ± 1.5; 1683 ± 153.3 versus 841.1 ± 72.3; 517 ± 50.5 versus 147 ± 8.7, respectively) and RSV+ PB (105.3 ± 18.1 versus 35.8 ± 4.1; 1683 ± 153.3 versus 818 ± 141.2; 517 ± 50.5 versus 260 ± 25.8, respectively). Furthermore, the percentage of neutrophils expressing Annexin V and the MFI of CD18 on neutrophils from RSV+ PB were increased compared with neutrophils from control PB. In addition, both CD11b (MFI) and CD18 (MFI) correlated with Annexin V (MFI) on neutrophils. We conclude that neutrophil apoptosis in RSV bronchiolitis is accelerated; and CD11b/CD18 may play an important role in RSV infection by influencing neutrophil apoptosis.</abstract><cop>Oxford BSL</cop><pub>Blackwell Science Ltd</pub><pmid>9764602</pmid><doi>10.1046/j.1365-2249.1998.00681.x</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Annexin A5 - biosynthesis Apoptosis Biological and medical sciences bronchiolitis Bronchiolitis - immunology Bronchiolitis - virology CD18 Antigens - biosynthesis fas Receptor - biosynthesis Human viral diseases Humans Infant Infectious diseases Macrophage-1 Antigen - biosynthesis Medical sciences neutrophil Neutrophils - metabolism Original regulation respiratory syncytial virus Respiratory Syncytial Virus Infections - immunology Respiratory Syncytial Virus, Human Viral diseases Viral diseases of the respiratory system and ent viral diseases |
title | The apoptosis of neutrophils is accelerated in respiratory syncytial virus (RSV)‐induced bronchiolitis |
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