IL-17–Induced Pulmonary Pathogenesis during Respiratory Viral Infection and Exacerbation of Allergic Disease
Severe respiratory syncytial virus (RSV) infections are characterized by airway epithelial cell damage, mucus hypersecretion, and Th2 cytokine production. Less is known about the role of IL-17. We observed increased IL-6 and IL-17 levels in tracheal aspirate samples from severely ill infants with RS...
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| description | Severe respiratory syncytial virus (RSV) infections are characterized by airway epithelial cell damage, mucus hypersecretion, and Th2 cytokine production. Less is known about the role of IL-17. We observed increased IL-6 and IL-17 levels in tracheal aspirate samples from severely ill infants with RSV infection. In a mouse model of RSV infection, time-dependent increases in pulmonary IL-6, IL-23, and IL-17 expression were observed. Neutralization of IL-17 during infection and observations from IL-17−/− knockout mice resulted in significant inhibition of mucus production during RSV infection. RSV-infected animals treated with anti-IL-17 had reduced inflammation and decreased viral load, compared with control antibody-treated mice. Blocking IL-17 during infection resulted in significantly increased RSV-specific CD8 T cells. Factors associated with CD8 cytotoxic T lymphocytes, T-bet, IFN-γ, eomesodermin, and granzyme B were significantly up-regulated after IL-17 blockade. Additionally, in vitro analyses suggest that IL-17 directly inhibits T-bet, eomesodermin, and IFN-γ in CD8 T cells. The role of IL-17 was also investigated in RSV-induced exacerbation of allergic airway responses, in which neutralization of IL-17 led to a significant decrease in the exacerbated disease, including reduced mucus production and Th2 cytokines, with decreased viral proteins. Taken together, our data demonstrate that IL-17 plays a pathogenic role during RSV infections. |
| doi_str_mv | 10.1016/j.ajpath.2011.03.003 |
| format | Article |
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Less is known about the role of IL-17. We observed increased IL-6 and IL-17 levels in tracheal aspirate samples from severely ill infants with RSV infection. In a mouse model of RSV infection, time-dependent increases in pulmonary IL-6, IL-23, and IL-17 expression were observed. Neutralization of IL-17 during infection and observations from IL-17−/− knockout mice resulted in significant inhibition of mucus production during RSV infection. RSV-infected animals treated with anti-IL-17 had reduced inflammation and decreased viral load, compared with control antibody-treated mice. Blocking IL-17 during infection resulted in significantly increased RSV-specific CD8 T cells. Factors associated with CD8 cytotoxic T lymphocytes, T-bet, IFN-γ, eomesodermin, and granzyme B were significantly up-regulated after IL-17 blockade. Additionally, in vitro analyses suggest that IL-17 directly inhibits T-bet, eomesodermin, and IFN-γ in CD8 T cells. The role of IL-17 was also investigated in RSV-induced exacerbation of allergic airway responses, in which neutralization of IL-17 led to a significant decrease in the exacerbated disease, including reduced mucus production and Th2 cytokines, with decreased viral proteins. Taken together, our data demonstrate that IL-17 plays a pathogenic role during RSV infections.</description><identifier>ISSN: 0002-9440</identifier><identifier>EISSN: 1525-2191</identifier><identifier>DOI: 10.1016/j.ajpath.2011.03.003</identifier><identifier>PMID: 21703407</identifier><identifier>CODEN: AJPAA4</identifier><language>eng</language><publisher>Bethesda, MD: Elsevier Inc</publisher><subject>Animals ; Antibodies, Monoclonal - pharmacology ; Biological and medical sciences ; Blotting, Western ; CD8-Positive T-Lymphocytes - metabolism ; CD8-Positive T-Lymphocytes - pathology ; CD8-Positive T-Lymphocytes - virology ; Disease Models, Animal ; Female ; Flow Cytometry ; Granzymes - genetics ; Granzymes - metabolism ; Humans ; Hypersensitivity - metabolism ; Hypersensitivity - pathology ; Hypersensitivity - virology ; Infectious diseases ; Inflammation - metabolism ; Inflammation - pathology ; Inflammation - virology ; Interferon-gamma - genetics ; Interferon-gamma - metabolism ; Interleukin-17 - physiology ; Interleukin-23 - metabolism ; Investigative techniques, diagnostic techniques (general aspects) ; Lung Diseases - metabolism ; Lung Diseases - pathology ; Lung Diseases - virology ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Mucus - metabolism ; Pathology ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; Regular ; Respiratory Syncytial Virus Infections - metabolism ; Respiratory Syncytial Virus Infections - pathology ; Respiratory Syncytial Virus Infections - virology ; Respiratory Syncytial Viruses - pathogenicity ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; T-Lymphocytes, Cytotoxic - metabolism ; T-Lymphocytes, Cytotoxic - pathology ; T-Lymphocytes, Cytotoxic - virology ; Viral diseases ; Viral Load ; Viral Proteins - metabolism</subject><ispartof>The American journal of pathology, 2011-07, Vol.179 (1), p.248-258</ispartof><rights>American Society for Investigative Pathology</rights><rights>2011 American Society for Investigative Pathology</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.</rights><rights>2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved. 2011 American Society for Investigative Pathology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c543t-3d4ecfa3c9981a422217f62db367e6ae69395492e35bb2c7e96e1b4f8bb779363</citedby><cites>FETCH-LOGICAL-c543t-3d4ecfa3c9981a422217f62db367e6ae69395492e35bb2c7e96e1b4f8bb779363</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/PMC3123803/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ajpath.2011.03.003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,724,777,781,882,3537,27905,27906,45976,53772,53774</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24317965$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21703407$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mukherjee, Sumanta</creatorcontrib><creatorcontrib>Lindell, Dennis M</creatorcontrib><creatorcontrib>Berlin, Aaron A</creatorcontrib><creatorcontrib>Morris, Susan B</creatorcontrib><creatorcontrib>Shanley, Thomas P</creatorcontrib><creatorcontrib>Hershenson, Marc B</creatorcontrib><creatorcontrib>Lukacs, Nicholas W</creatorcontrib><title>IL-17–Induced Pulmonary Pathogenesis during Respiratory Viral Infection and Exacerbation of Allergic Disease</title><title>The American journal of pathology</title><addtitle>Am J Pathol</addtitle><description>Severe respiratory syncytial virus (RSV) infections are characterized by airway epithelial cell damage, mucus hypersecretion, and Th2 cytokine production. Less is known about the role of IL-17. We observed increased IL-6 and IL-17 levels in tracheal aspirate samples from severely ill infants with RSV infection. In a mouse model of RSV infection, time-dependent increases in pulmonary IL-6, IL-23, and IL-17 expression were observed. Neutralization of IL-17 during infection and observations from IL-17−/− knockout mice resulted in significant inhibition of mucus production during RSV infection. RSV-infected animals treated with anti-IL-17 had reduced inflammation and decreased viral load, compared with control antibody-treated mice. Blocking IL-17 during infection resulted in significantly increased RSV-specific CD8 T cells. Factors associated with CD8 cytotoxic T lymphocytes, T-bet, IFN-γ, eomesodermin, and granzyme B were significantly up-regulated after IL-17 blockade. Additionally, in vitro analyses suggest that IL-17 directly inhibits T-bet, eomesodermin, and IFN-γ in CD8 T cells. The role of IL-17 was also investigated in RSV-induced exacerbation of allergic airway responses, in which neutralization of IL-17 led to a significant decrease in the exacerbated disease, including reduced mucus production and Th2 cytokines, with decreased viral proteins. Taken together, our data demonstrate that IL-17 plays a pathogenic role during RSV infections.</description><subject>Animals</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>CD8-Positive T-Lymphocytes - metabolism</subject><subject>CD8-Positive T-Lymphocytes - pathology</subject><subject>CD8-Positive T-Lymphocytes - virology</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Granzymes - genetics</subject><subject>Granzymes - metabolism</subject><subject>Humans</subject><subject>Hypersensitivity - metabolism</subject><subject>Hypersensitivity - pathology</subject><subject>Hypersensitivity - virology</subject><subject>Infectious diseases</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Inflammation - virology</subject><subject>Interferon-gamma - genetics</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin-17 - physiology</subject><subject>Interleukin-23 - metabolism</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Lung Diseases - metabolism</subject><subject>Lung Diseases - pathology</subject><subject>Lung Diseases - virology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Knockout</subject><subject>Mucus - metabolism</subject><subject>Pathology</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>Regular</subject><subject>Respiratory Syncytial Virus Infections - metabolism</subject><subject>Respiratory Syncytial Virus Infections - pathology</subject><subject>Respiratory Syncytial Virus Infections - virology</subject><subject>Respiratory Syncytial Viruses - pathogenicity</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>T-Lymphocytes, Cytotoxic - metabolism</subject><subject>T-Lymphocytes, Cytotoxic - pathology</subject><subject>T-Lymphocytes, Cytotoxic - virology</subject><subject>Viral diseases</subject><subject>Viral Load</subject><subject>Viral Proteins - metabolism</subject><issn>0002-9440</issn><issn>1525-2191</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUk1v1DAQtRCILoV_gFAuHBM8tuOsL0hVW2Cllaj4ulqOM9k6ZO2VnVT0xn_gH_JL8HZLC1w4-WPeezPzZgh5DrQCCvLVUJlhZ6bLilGAivKKUv6ALKBmdclAwUOyoJSyUglBj8iTlIb8lHxJH5MjBg3lgjYL4lfrEpqf33-sfDdb7IqLedwGb-J1cZHFwwY9JpeKbo7Ob4oPmHYumink-Jd8GYuV79FOLvjC-K44_2YsxtbcfIS-OBlHjBtnizOX0CR8Sh71Zkz47PY8Jp_fnH86fVeu379dnZ6sS1sLPpW8E2h7w61SSzCCsVxwL1nXctmgNCgVV7VQDHndtsw2qCRCK_pl2zaN4pIfk9cH3d3cbrGz6KdcrN5Ft82t6WCc_jvi3aXehCvNgWWLeBYQBwEbQ0oR-zsuUL33Xw_64L_e-68p1_SG9uLPvHek34ZnwMtbgEnWjH003rp0jxMcGiXr-wYwu3TlMOpkHfo8IRez37oL7n-V_CtgR-ddzvkVrzENYY4-T0CDTkxT_XG_K_tVAchskJL_AlS8vTo</recordid><startdate>20110701</startdate><enddate>20110701</enddate><creator>Mukherjee, Sumanta</creator><creator>Lindell, Dennis M</creator><creator>Berlin, Aaron A</creator><creator>Morris, Susan B</creator><creator>Shanley, Thomas P</creator><creator>Hershenson, Marc B</creator><creator>Lukacs, Nicholas W</creator><general>Elsevier Inc</general><general>American Society for Investigative Pathology</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>5PM</scope></search><sort><creationdate>20110701</creationdate><title>IL-17–Induced Pulmonary Pathogenesis during Respiratory Viral Infection and Exacerbation of Allergic Disease</title><author>Mukherjee, Sumanta ; Lindell, Dennis M ; Berlin, Aaron A ; Morris, Susan B ; Shanley, Thomas P ; Hershenson, Marc B ; Lukacs, Nicholas W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c543t-3d4ecfa3c9981a422217f62db367e6ae69395492e35bb2c7e96e1b4f8bb779363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>CD8-Positive T-Lymphocytes - metabolism</topic><topic>CD8-Positive T-Lymphocytes - pathology</topic><topic>CD8-Positive T-Lymphocytes - virology</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Granzymes - genetics</topic><topic>Granzymes - metabolism</topic><topic>Humans</topic><topic>Hypersensitivity - metabolism</topic><topic>Hypersensitivity - pathology</topic><topic>Hypersensitivity - virology</topic><topic>Infectious diseases</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Inflammation - virology</topic><topic>Interferon-gamma - genetics</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukin-17 - physiology</topic><topic>Interleukin-23 - metabolism</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Lung Diseases - metabolism</topic><topic>Lung Diseases - pathology</topic><topic>Lung Diseases - virology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Knockout</topic><topic>Mucus - metabolism</topic><topic>Pathology</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. 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Less is known about the role of IL-17. We observed increased IL-6 and IL-17 levels in tracheal aspirate samples from severely ill infants with RSV infection. In a mouse model of RSV infection, time-dependent increases in pulmonary IL-6, IL-23, and IL-17 expression were observed. Neutralization of IL-17 during infection and observations from IL-17−/− knockout mice resulted in significant inhibition of mucus production during RSV infection. RSV-infected animals treated with anti-IL-17 had reduced inflammation and decreased viral load, compared with control antibody-treated mice. Blocking IL-17 during infection resulted in significantly increased RSV-specific CD8 T cells. Factors associated with CD8 cytotoxic T lymphocytes, T-bet, IFN-γ, eomesodermin, and granzyme B were significantly up-regulated after IL-17 blockade. Additionally, in vitro analyses suggest that IL-17 directly inhibits T-bet, eomesodermin, and IFN-γ in CD8 T cells. The role of IL-17 was also investigated in RSV-induced exacerbation of allergic airway responses, in which neutralization of IL-17 led to a significant decrease in the exacerbated disease, including reduced mucus production and Th2 cytokines, with decreased viral proteins. Taken together, our data demonstrate that IL-17 plays a pathogenic role during RSV infections.</abstract><cop>Bethesda, MD</cop><pub>Elsevier Inc</pub><pmid>21703407</pmid><doi>10.1016/j.ajpath.2011.03.003</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antibodies, Monoclonal - pharmacology Biological and medical sciences Blotting, Western CD8-Positive T-Lymphocytes - metabolism CD8-Positive T-Lymphocytes - pathology CD8-Positive T-Lymphocytes - virology Disease Models, Animal Female Flow Cytometry Granzymes - genetics Granzymes - metabolism Humans Hypersensitivity - metabolism Hypersensitivity - pathology Hypersensitivity - virology Infectious diseases Inflammation - metabolism Inflammation - pathology Inflammation - virology Interferon-gamma - genetics Interferon-gamma - metabolism Interleukin-17 - physiology Interleukin-23 - metabolism Investigative techniques, diagnostic techniques (general aspects) Lung Diseases - metabolism Lung Diseases - pathology Lung Diseases - virology Medical sciences Mice Mice, Inbred BALB C Mice, Knockout Mucus - metabolism Pathology Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Regular Respiratory Syncytial Virus Infections - metabolism Respiratory Syncytial Virus Infections - pathology Respiratory Syncytial Virus Infections - virology Respiratory Syncytial Viruses - pathogenicity Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics T-Lymphocytes, Cytotoxic - metabolism T-Lymphocytes, Cytotoxic - pathology T-Lymphocytes, Cytotoxic - virology Viral diseases Viral Load Viral Proteins - metabolism |
| title | IL-17–Induced Pulmonary Pathogenesis during Respiratory Viral Infection and Exacerbation of Allergic Disease |
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