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Role of S100A9 in the development of neutrophilic inflammation in asthmatics and in a murine model
S100A9 is an endogenous danger signal that promotes and exacerbates the neutrophilic inflammatory response. To investigate the role of S100A9 in neutrophilic asthma, S100A9 levels were measured in sputum from 101 steroid-naïve asthmatics using an ELISA kit and the levels were significantly correlate...
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Published in: | Clinical immunology (Orlando, Fla.) Fla.), 2017-10, Vol.183, p.158-166 |
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creator | Lee, Tae-Hyeong Chang, Hun Soo Bae, Da-Jeong Song, Hyun Ji Kim, Myung-Sin Park, Jong Sook Jun, Ji Ae Lee, Si Young Uh, Soo Taek Kim, Soo Hyun Park, Choon-Sik |
description | S100A9 is an endogenous danger signal that promotes and exacerbates the neutrophilic inflammatory response. To investigate the role of S100A9 in neutrophilic asthma, S100A9 levels were measured in sputum from 101 steroid-naïve asthmatics using an ELISA kit and the levels were significantly correlated with percentages of neutrophils in sputum. Intranasal administration of recombinant S100A9 markedly increased neutrophil numbers at 8h and 24h later with concomitant elevation of IL-1β, IL-17, and IFN-γ levels. Treatment with an anti-S100A9 antibody restored the increased numbers of neutrophils and the increased airway resistance in OVA/CFA mice toward the levels of sham-treated mice. Concomitantly, the S100A9 and neutrophil elastase double positive cells were markedly reduced with attenuation of IL-1β, IL-17, and IFN-γ levels by the treatment with the anti-S100A9 antibody. Our data support a role of S100A9 to initiate and amplify the neutrophilic inflammation in asthma, possibly via inducing IL-1β, IL-17 and IFN-γ.
•S100A9 is an endogenous danger signal that promotes and exacerbates the neutrophilic inflammatory response.•Our data support a role of S100A9 to initiate and amplify the neutrophilic inflammation via inducing IL-1β, IL-17 and IFN-γ.•Modulation of S100A9 in the airway may be a therapeutic strategy to control neutrophilic inflammation in asthma. |
doi_str_mv | 10.1016/j.clim.2017.08.013 |
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•S100A9 is an endogenous danger signal that promotes and exacerbates the neutrophilic inflammatory response.•Our data support a role of S100A9 to initiate and amplify the neutrophilic inflammation via inducing IL-1β, IL-17 and IFN-γ.•Modulation of S100A9 in the airway may be a therapeutic strategy to control neutrophilic inflammation in asthma.</description><identifier>ISSN: 1521-6616</identifier><identifier>EISSN: 1521-7035</identifier><identifier>DOI: 10.1016/j.clim.2017.08.013</identifier><identifier>PMID: 28847516</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adult ; Animals ; Antibodies, Neutralizing - pharmacology ; Asthma ; Asthma - immunology ; Asthma - physiopathology ; Calgranulin B ; Calgranulin B - immunology ; Disease Models, Animal ; Female ; Humans ; IFN-γ ; IL-17 ; IL-1β ; Inflammation ; Interferon-gamma - drug effects ; Interferon-gamma - immunology ; Interleukin-17 - immunology ; Interleukin-1beta - drug effects ; Interleukin-1beta - immunology ; Leukocyte Elastase - metabolism ; Male ; Mice ; Middle Aged ; Neutrophils - drug effects ; Neutrophils - immunology ; S100A9 ; Sputum - chemistry ; Sputum - immunology</subject><ispartof>Clinical immunology (Orlando, Fla.), 2017-10, Vol.183, p.158-166</ispartof><rights>2017 Elsevier Inc.</rights><rights>Copyright © 2017 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-3ec01ee0d7f7397d16ca967d94d42af54d18affb27bc0dbef544b8111e0ddd303</citedby><cites>FETCH-LOGICAL-c356t-3ec01ee0d7f7397d16ca967d94d42af54d18affb27bc0dbef544b8111e0ddd303</cites><orcidid>0000-0003-2453-6689 ; 0000-0002-4025-4182</orcidid></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/28847516$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Tae-Hyeong</creatorcontrib><creatorcontrib>Chang, Hun Soo</creatorcontrib><creatorcontrib>Bae, Da-Jeong</creatorcontrib><creatorcontrib>Song, Hyun Ji</creatorcontrib><creatorcontrib>Kim, Myung-Sin</creatorcontrib><creatorcontrib>Park, Jong Sook</creatorcontrib><creatorcontrib>Jun, Ji Ae</creatorcontrib><creatorcontrib>Lee, Si Young</creatorcontrib><creatorcontrib>Uh, Soo Taek</creatorcontrib><creatorcontrib>Kim, Soo Hyun</creatorcontrib><creatorcontrib>Park, Choon-Sik</creatorcontrib><title>Role of S100A9 in the development of neutrophilic inflammation in asthmatics and in a murine model</title><title>Clinical immunology (Orlando, Fla.)</title><addtitle>Clin Immunol</addtitle><description>S100A9 is an endogenous danger signal that promotes and exacerbates the neutrophilic inflammatory response. To investigate the role of S100A9 in neutrophilic asthma, S100A9 levels were measured in sputum from 101 steroid-naïve asthmatics using an ELISA kit and the levels were significantly correlated with percentages of neutrophils in sputum. Intranasal administration of recombinant S100A9 markedly increased neutrophil numbers at 8h and 24h later with concomitant elevation of IL-1β, IL-17, and IFN-γ levels. Treatment with an anti-S100A9 antibody restored the increased numbers of neutrophils and the increased airway resistance in OVA/CFA mice toward the levels of sham-treated mice. Concomitantly, the S100A9 and neutrophil elastase double positive cells were markedly reduced with attenuation of IL-1β, IL-17, and IFN-γ levels by the treatment with the anti-S100A9 antibody. Our data support a role of S100A9 to initiate and amplify the neutrophilic inflammation in asthma, possibly via inducing IL-1β, IL-17 and IFN-γ.
•S100A9 is an endogenous danger signal that promotes and exacerbates the neutrophilic inflammatory response.•Our data support a role of S100A9 to initiate and amplify the neutrophilic inflammation via inducing IL-1β, IL-17 and IFN-γ.•Modulation of S100A9 in the airway may be a therapeutic strategy to control neutrophilic inflammation in asthma.</description><subject>Adult</subject><subject>Animals</subject><subject>Antibodies, Neutralizing - pharmacology</subject><subject>Asthma</subject><subject>Asthma - immunology</subject><subject>Asthma - physiopathology</subject><subject>Calgranulin B</subject><subject>Calgranulin B - immunology</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Humans</subject><subject>IFN-γ</subject><subject>IL-17</subject><subject>IL-1β</subject><subject>Inflammation</subject><subject>Interferon-gamma - drug effects</subject><subject>Interferon-gamma - immunology</subject><subject>Interleukin-17 - immunology</subject><subject>Interleukin-1beta - drug effects</subject><subject>Interleukin-1beta - immunology</subject><subject>Leukocyte Elastase - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Middle Aged</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - immunology</subject><subject>S100A9</subject><subject>Sputum - chemistry</subject><subject>Sputum - immunology</subject><issn>1521-6616</issn><issn>1521-7035</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp9kMFq3DAQhkVJ6CZpX6CH4mMu68xYtmxDL8uStoFAIG3PQpbGrBbJ2kr2Qt4-dnebY06SRt__w3yMfUHIEVDc7XPtrM8LwDqHJgfkH9gVVgWua-DVxfkuBIoVu05pDwBVUYiPbFU0TVlXKK5Y9xwcZaHPfiHAps3skI07ygwdyYWDp2FcPgeaxhgOO-usnpHeKe_VaMOw8CqNu-WlU6YG82-S-SnagTIfDLlP7LJXLtHn83nD_ny__739uX58-vGw3TyuNa_EuOakAYnA1H3N29qg0KoVtWlLUxaqr0qDjer7rqg7DaajeVJ2DSLOEWM48Bt2e-o9xPB3ojRKb5Mm59RAYUoSW84FiJLjjBYnVMeQUqReHqL1Kr5IBLm4lXu5uJWLWwmNnN3Ooa_n_qnzZN4i_2XOwLcTQPOWR0tRJm1p0GRsJD1KE-x7_a-HIor8</recordid><startdate>201710</startdate><enddate>201710</enddate><creator>Lee, Tae-Hyeong</creator><creator>Chang, Hun Soo</creator><creator>Bae, Da-Jeong</creator><creator>Song, Hyun Ji</creator><creator>Kim, Myung-Sin</creator><creator>Park, Jong Sook</creator><creator>Jun, Ji Ae</creator><creator>Lee, Si Young</creator><creator>Uh, Soo Taek</creator><creator>Kim, Soo Hyun</creator><creator>Park, Choon-Sik</creator><general>Elsevier Inc</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>7X8</scope><orcidid>https://orcid.org/0000-0003-2453-6689</orcidid><orcidid>https://orcid.org/0000-0002-4025-4182</orcidid></search><sort><creationdate>201710</creationdate><title>Role of S100A9 in the development of neutrophilic inflammation in asthmatics and in a murine model</title><author>Lee, Tae-Hyeong ; Chang, Hun Soo ; Bae, Da-Jeong ; Song, Hyun Ji ; Kim, Myung-Sin ; Park, Jong Sook ; Jun, Ji Ae ; Lee, Si Young ; Uh, Soo Taek ; Kim, Soo Hyun ; Park, Choon-Sik</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-3ec01ee0d7f7397d16ca967d94d42af54d18affb27bc0dbef544b8111e0ddd303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Animals</topic><topic>Antibodies, Neutralizing - pharmacology</topic><topic>Asthma</topic><topic>Asthma - immunology</topic><topic>Asthma - physiopathology</topic><topic>Calgranulin B</topic><topic>Calgranulin B - immunology</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Humans</topic><topic>IFN-γ</topic><topic>IL-17</topic><topic>IL-1β</topic><topic>Inflammation</topic><topic>Interferon-gamma - drug effects</topic><topic>Interferon-gamma - immunology</topic><topic>Interleukin-17 - immunology</topic><topic>Interleukin-1beta - drug effects</topic><topic>Interleukin-1beta - immunology</topic><topic>Leukocyte Elastase - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Middle Aged</topic><topic>Neutrophils - drug effects</topic><topic>Neutrophils - immunology</topic><topic>S100A9</topic><topic>Sputum - chemistry</topic><topic>Sputum - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Tae-Hyeong</creatorcontrib><creatorcontrib>Chang, Hun Soo</creatorcontrib><creatorcontrib>Bae, Da-Jeong</creatorcontrib><creatorcontrib>Song, Hyun Ji</creatorcontrib><creatorcontrib>Kim, Myung-Sin</creatorcontrib><creatorcontrib>Park, Jong Sook</creatorcontrib><creatorcontrib>Jun, Ji Ae</creatorcontrib><creatorcontrib>Lee, Si Young</creatorcontrib><creatorcontrib>Uh, Soo Taek</creatorcontrib><creatorcontrib>Kim, Soo Hyun</creatorcontrib><creatorcontrib>Park, Choon-Sik</creatorcontrib><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><jtitle>Clinical immunology (Orlando, Fla.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Tae-Hyeong</au><au>Chang, Hun Soo</au><au>Bae, Da-Jeong</au><au>Song, Hyun Ji</au><au>Kim, Myung-Sin</au><au>Park, Jong Sook</au><au>Jun, Ji Ae</au><au>Lee, Si Young</au><au>Uh, Soo Taek</au><au>Kim, Soo Hyun</au><au>Park, Choon-Sik</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of S100A9 in the development of neutrophilic inflammation in asthmatics and in a murine model</atitle><jtitle>Clinical immunology (Orlando, Fla.)</jtitle><addtitle>Clin Immunol</addtitle><date>2017-10</date><risdate>2017</risdate><volume>183</volume><spage>158</spage><epage>166</epage><pages>158-166</pages><issn>1521-6616</issn><eissn>1521-7035</eissn><abstract>S100A9 is an endogenous danger signal that promotes and exacerbates the neutrophilic inflammatory response. To investigate the role of S100A9 in neutrophilic asthma, S100A9 levels were measured in sputum from 101 steroid-naïve asthmatics using an ELISA kit and the levels were significantly correlated with percentages of neutrophils in sputum. Intranasal administration of recombinant S100A9 markedly increased neutrophil numbers at 8h and 24h later with concomitant elevation of IL-1β, IL-17, and IFN-γ levels. Treatment with an anti-S100A9 antibody restored the increased numbers of neutrophils and the increased airway resistance in OVA/CFA mice toward the levels of sham-treated mice. Concomitantly, the S100A9 and neutrophil elastase double positive cells were markedly reduced with attenuation of IL-1β, IL-17, and IFN-γ levels by the treatment with the anti-S100A9 antibody. Our data support a role of S100A9 to initiate and amplify the neutrophilic inflammation in asthma, possibly via inducing IL-1β, IL-17 and IFN-γ.
•S100A9 is an endogenous danger signal that promotes and exacerbates the neutrophilic inflammatory response.•Our data support a role of S100A9 to initiate and amplify the neutrophilic inflammation via inducing IL-1β, IL-17 and IFN-γ.•Modulation of S100A9 in the airway may be a therapeutic strategy to control neutrophilic inflammation in asthma.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>28847516</pmid><doi>10.1016/j.clim.2017.08.013</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-2453-6689</orcidid><orcidid>https://orcid.org/0000-0002-4025-4182</orcidid></addata></record> |
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subjects | Adult Animals Antibodies, Neutralizing - pharmacology Asthma Asthma - immunology Asthma - physiopathology Calgranulin B Calgranulin B - immunology Disease Models, Animal Female Humans IFN-γ IL-17 IL-1β Inflammation Interferon-gamma - drug effects Interferon-gamma - immunology Interleukin-17 - immunology Interleukin-1beta - drug effects Interleukin-1beta - immunology Leukocyte Elastase - metabolism Male Mice Middle Aged Neutrophils - drug effects Neutrophils - immunology S100A9 Sputum - chemistry Sputum - immunology |
title | Role of S100A9 in the development of neutrophilic inflammation in asthmatics and in a murine model |
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