Cysteinyl leukotriene receptor 1 expression identifies a subset of neutrophils during the antiviral response that contributes to postviral atopic airway disease
Viral respiratory tract infections increase the risk of development and exacerbation of atopic disease. Previously, we demonstrated the requirement for a neutrophil (PMN) subset expressing CD49d to drive development of postviral atopic airway disease in mice. We sought to determine whether human CD4...
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| Veröffentlicht in: | Journal of allergy and clinical immunology 2018-10, Vol.142 (4), p.1206-1217.e5 |
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| creator | Cheung, Dorothy S. Sigua, Jerome A. Simpson, Pippa M. Yan, Ke Hussain, Syed-Rehan A. Santoro, Jennifer L. Buell, Erika J. Hunter, Desire A. Rohlfing, Michelle Patadia, Deepa Grayson, Mitchell H. |
| description | Viral respiratory tract infections increase the risk of development and exacerbation of atopic disease. Previously, we demonstrated the requirement for a neutrophil (PMN) subset expressing CD49d to drive development of postviral atopic airway disease in mice.
We sought to determine whether human CD49d+ PMNs are present in the nasal mucosa during acute viral respiratory tract infections and further characterize this PMN subset in human subjects and mice.
Sixty subjects (5-50 years old) were enrolled within 4 days of acute onset of upper respiratory symptoms. Nasal lavage for flow cytometry and nasal swabs for viral PCR were performed at enrollment and during convalescence. The Sendai virus mouse model was used to investigate the phenotype and functional relevance of CD49d+ PMNs.
CD49d+ PMN frequency was significantly higher in nasal lavage fluid during acute respiratory symptoms in all subjects (2.9% vs 1.0%, n = 42, P |
| doi_str_mv | 10.1016/j.jaci.2017.11.026 |
| format | Article |
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We sought to determine whether human CD49d+ PMNs are present in the nasal mucosa during acute viral respiratory tract infections and further characterize this PMN subset in human subjects and mice.
Sixty subjects (5-50 years old) were enrolled within 4 days of acute onset of upper respiratory symptoms. Nasal lavage for flow cytometry and nasal swabs for viral PCR were performed at enrollment and during convalescence. The Sendai virus mouse model was used to investigate the phenotype and functional relevance of CD49d+ PMNs.
CD49d+ PMN frequency was significantly higher in nasal lavage fluid during acute respiratory symptoms in all subjects (2.9% vs 1.0%, n = 42, P < .001). In mice CD49d+ PMNs represented a “proatopic” neutrophil subset that expressed cysteinyl leukotriene receptor 1 (CysLTR1) and produced TNF, CCL2, and CCL5. Inhibition of CysLTR1 signaling in the first days of a viral respiratory tract infection was sufficient to reduce accumulation of CD49d+ PMNs in the lungs and development of postviral atopic airway disease. Similar to the mouse, human CD49d+ PMNs isolated from nasal lavage fluid during a viral respiratory tract infection expressed CysLTR1.
CD49d and CysLTR1–coexpressing PMNs are present during symptoms of an acute viral respiratory tract infection in human subjects. Further study is needed to examine selective targeting of proatopic neutrophils as a potential therapeutic strategy to prevent development of postviral atopic airway disease.
[Display omitted]</description><identifier>ISSN: 0091-6749</identifier><identifier>EISSN: 1097-6825</identifier><identifier>DOI: 10.1016/j.jaci.2017.11.026</identifier><identifier>PMID: 29269317</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Antiviral drugs ; Asthma ; Atopy ; CD49d antigen ; Children & youth ; Convalescence ; cysteinyl leukotrienes ; Dendritic cells ; Disease ; Flow cytometry ; Health risks ; Hospitals ; Human subjects ; Infections ; Influenza ; Leukocytes (neutrophilic) ; Mice ; Monocyte chemoattractant protein 1 ; Mucosa ; nasal lavage ; Neutrophils ; Phenotypes ; Respiratory syncytial virus ; Respiratory tract ; Respiratory tract diseases ; Software ; viral infection ; Viral infections ; Viruses</subject><ispartof>Journal of allergy and clinical immunology, 2018-10, Vol.142 (4), p.1206-1217.e5</ispartof><rights>2017 American Academy of Allergy, Asthma & Immunology</rights><rights>Copyright © 2017 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Oct 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c428t-ff01fd38f92b1502b130efd4546dd9210cbd10a2f648ac9869c8a0acd44430833</citedby><cites>FETCH-LOGICAL-c428t-ff01fd38f92b1502b130efd4546dd9210cbd10a2f648ac9869c8a0acd44430833</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0091674917329135$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29269317$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheung, Dorothy S.</creatorcontrib><creatorcontrib>Sigua, Jerome A.</creatorcontrib><creatorcontrib>Simpson, Pippa M.</creatorcontrib><creatorcontrib>Yan, Ke</creatorcontrib><creatorcontrib>Hussain, Syed-Rehan A.</creatorcontrib><creatorcontrib>Santoro, Jennifer L.</creatorcontrib><creatorcontrib>Buell, Erika J.</creatorcontrib><creatorcontrib>Hunter, Desire A.</creatorcontrib><creatorcontrib>Rohlfing, Michelle</creatorcontrib><creatorcontrib>Patadia, Deepa</creatorcontrib><creatorcontrib>Grayson, Mitchell H.</creatorcontrib><title>Cysteinyl leukotriene receptor 1 expression identifies a subset of neutrophils during the antiviral response that contributes to postviral atopic airway disease</title><title>Journal of allergy and clinical immunology</title><addtitle>J Allergy Clin Immunol</addtitle><description>Viral respiratory tract infections increase the risk of development and exacerbation of atopic disease. Previously, we demonstrated the requirement for a neutrophil (PMN) subset expressing CD49d to drive development of postviral atopic airway disease in mice.
We sought to determine whether human CD49d+ PMNs are present in the nasal mucosa during acute viral respiratory tract infections and further characterize this PMN subset in human subjects and mice.
Sixty subjects (5-50 years old) were enrolled within 4 days of acute onset of upper respiratory symptoms. Nasal lavage for flow cytometry and nasal swabs for viral PCR were performed at enrollment and during convalescence. The Sendai virus mouse model was used to investigate the phenotype and functional relevance of CD49d+ PMNs.
CD49d+ PMN frequency was significantly higher in nasal lavage fluid during acute respiratory symptoms in all subjects (2.9% vs 1.0%, n = 42, P < .001). In mice CD49d+ PMNs represented a “proatopic” neutrophil subset that expressed cysteinyl leukotriene receptor 1 (CysLTR1) and produced TNF, CCL2, and CCL5. Inhibition of CysLTR1 signaling in the first days of a viral respiratory tract infection was sufficient to reduce accumulation of CD49d+ PMNs in the lungs and development of postviral atopic airway disease. Similar to the mouse, human CD49d+ PMNs isolated from nasal lavage fluid during a viral respiratory tract infection expressed CysLTR1.
CD49d and CysLTR1–coexpressing PMNs are present during symptoms of an acute viral respiratory tract infection in human subjects. Further study is needed to examine selective targeting of proatopic neutrophils as a potential therapeutic strategy to prevent development of postviral atopic airway disease.
[Display omitted]</description><subject>Antiviral drugs</subject><subject>Asthma</subject><subject>Atopy</subject><subject>CD49d antigen</subject><subject>Children & youth</subject><subject>Convalescence</subject><subject>cysteinyl leukotrienes</subject><subject>Dendritic cells</subject><subject>Disease</subject><subject>Flow cytometry</subject><subject>Health risks</subject><subject>Hospitals</subject><subject>Human subjects</subject><subject>Infections</subject><subject>Influenza</subject><subject>Leukocytes (neutrophilic)</subject><subject>Mice</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Mucosa</subject><subject>nasal lavage</subject><subject>Neutrophils</subject><subject>Phenotypes</subject><subject>Respiratory syncytial virus</subject><subject>Respiratory tract</subject><subject>Respiratory tract diseases</subject><subject>Software</subject><subject>viral infection</subject><subject>Viral infections</subject><subject>Viruses</subject><issn>0091-6749</issn><issn>1097-6825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp9kcFu1DAQhi0EotvCC3BAlrhwyeJxskkscUEroEiVuMDZcuwJdcjaweO07NvwqHi1hQMHLh559M1vaz7GXoDYgoD2zbSdjPVbKaDbAmyFbB-xDQjVVW0vd4_ZRggFVds16oJdEk2i3OtePWUXUslW1dBt2K_9kTL6cJz5jOv3mJPHgDyhxSXHxIHjzyUhkY-Be4ch-9EjccNpHQgzjyMPuOYUl1s_E3dr8uEbz7fITWHvfDJzSaMlBsLSNpnbGMorw5pLTI58iZTPmMlx8ZYbn-7NkTtPaAifsSejmQmfP9Qr9vXD-y_76-rm88dP-3c3lW1kn6txFDC6uh-VHGAnylELHF2za1rnlARhBwfCyLFtemNV3yrbG2Gsa5qmFn1dX7HX59wlxR8rUtYHTxbn2QSMK2lQnVJtB0IW9NU_6BTXFMrvtARoy5aVFIWSZ8qmSJRw1EvyB5OOGoQ--dOTPvnTJ38aQBd_ZejlQ_Q6HND9HfkjrABvzwCWXdx5TJpsMWbR-eIsaxf9__J_AxB5sBs</recordid><startdate>201810</startdate><enddate>201810</enddate><creator>Cheung, Dorothy S.</creator><creator>Sigua, Jerome A.</creator><creator>Simpson, Pippa M.</creator><creator>Yan, Ke</creator><creator>Hussain, Syed-Rehan A.</creator><creator>Santoro, Jennifer L.</creator><creator>Buell, Erika J.</creator><creator>Hunter, Desire A.</creator><creator>Rohlfing, Michelle</creator><creator>Patadia, Deepa</creator><creator>Grayson, Mitchell H.</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7SS</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>201810</creationdate><title>Cysteinyl leukotriene receptor 1 expression identifies a subset of neutrophils during the antiviral response that contributes to postviral atopic airway disease</title><author>Cheung, Dorothy S. ; Sigua, Jerome A. ; Simpson, Pippa M. ; Yan, Ke ; Hussain, Syed-Rehan A. ; Santoro, Jennifer L. ; Buell, Erika J. ; Hunter, Desire A. ; Rohlfing, Michelle ; Patadia, Deepa ; Grayson, Mitchell H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c428t-ff01fd38f92b1502b130efd4546dd9210cbd10a2f648ac9869c8a0acd44430833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Antiviral drugs</topic><topic>Asthma</topic><topic>Atopy</topic><topic>CD49d antigen</topic><topic>Children & youth</topic><topic>Convalescence</topic><topic>cysteinyl leukotrienes</topic><topic>Dendritic cells</topic><topic>Disease</topic><topic>Flow cytometry</topic><topic>Health risks</topic><topic>Hospitals</topic><topic>Human subjects</topic><topic>Infections</topic><topic>Influenza</topic><topic>Leukocytes (neutrophilic)</topic><topic>Mice</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Mucosa</topic><topic>nasal lavage</topic><topic>Neutrophils</topic><topic>Phenotypes</topic><topic>Respiratory syncytial virus</topic><topic>Respiratory tract</topic><topic>Respiratory tract diseases</topic><topic>Software</topic><topic>viral infection</topic><topic>Viral infections</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheung, Dorothy S.</creatorcontrib><creatorcontrib>Sigua, Jerome A.</creatorcontrib><creatorcontrib>Simpson, Pippa M.</creatorcontrib><creatorcontrib>Yan, Ke</creatorcontrib><creatorcontrib>Hussain, Syed-Rehan A.</creatorcontrib><creatorcontrib>Santoro, Jennifer L.</creatorcontrib><creatorcontrib>Buell, Erika J.</creatorcontrib><creatorcontrib>Hunter, Desire A.</creatorcontrib><creatorcontrib>Rohlfing, Michelle</creatorcontrib><creatorcontrib>Patadia, Deepa</creatorcontrib><creatorcontrib>Grayson, Mitchell H.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of allergy and clinical immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheung, Dorothy S.</au><au>Sigua, Jerome A.</au><au>Simpson, Pippa M.</au><au>Yan, Ke</au><au>Hussain, Syed-Rehan A.</au><au>Santoro, Jennifer L.</au><au>Buell, Erika J.</au><au>Hunter, Desire A.</au><au>Rohlfing, Michelle</au><au>Patadia, Deepa</au><au>Grayson, Mitchell H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cysteinyl leukotriene receptor 1 expression identifies a subset of neutrophils during the antiviral response that contributes to postviral atopic airway disease</atitle><jtitle>Journal of allergy and clinical immunology</jtitle><addtitle>J Allergy Clin Immunol</addtitle><date>2018-10</date><risdate>2018</risdate><volume>142</volume><issue>4</issue><spage>1206</spage><epage>1217.e5</epage><pages>1206-1217.e5</pages><issn>0091-6749</issn><eissn>1097-6825</eissn><abstract>Viral respiratory tract infections increase the risk of development and exacerbation of atopic disease. Previously, we demonstrated the requirement for a neutrophil (PMN) subset expressing CD49d to drive development of postviral atopic airway disease in mice.
We sought to determine whether human CD49d+ PMNs are present in the nasal mucosa during acute viral respiratory tract infections and further characterize this PMN subset in human subjects and mice.
Sixty subjects (5-50 years old) were enrolled within 4 days of acute onset of upper respiratory symptoms. Nasal lavage for flow cytometry and nasal swabs for viral PCR were performed at enrollment and during convalescence. The Sendai virus mouse model was used to investigate the phenotype and functional relevance of CD49d+ PMNs.
CD49d+ PMN frequency was significantly higher in nasal lavage fluid during acute respiratory symptoms in all subjects (2.9% vs 1.0%, n = 42, P < .001). In mice CD49d+ PMNs represented a “proatopic” neutrophil subset that expressed cysteinyl leukotriene receptor 1 (CysLTR1) and produced TNF, CCL2, and CCL5. Inhibition of CysLTR1 signaling in the first days of a viral respiratory tract infection was sufficient to reduce accumulation of CD49d+ PMNs in the lungs and development of postviral atopic airway disease. Similar to the mouse, human CD49d+ PMNs isolated from nasal lavage fluid during a viral respiratory tract infection expressed CysLTR1.
CD49d and CysLTR1–coexpressing PMNs are present during symptoms of an acute viral respiratory tract infection in human subjects. Further study is needed to examine selective targeting of proatopic neutrophils as a potential therapeutic strategy to prevent development of postviral atopic airway disease.
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| subjects | Antiviral drugs Asthma Atopy CD49d antigen Children & youth Convalescence cysteinyl leukotrienes Dendritic cells Disease Flow cytometry Health risks Hospitals Human subjects Infections Influenza Leukocytes (neutrophilic) Mice Monocyte chemoattractant protein 1 Mucosa nasal lavage Neutrophils Phenotypes Respiratory syncytial virus Respiratory tract Respiratory tract diseases Software viral infection Viral infections Viruses |
| title | Cysteinyl leukotriene receptor 1 expression identifies a subset of neutrophils during the antiviral response that contributes to postviral atopic airway disease |
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