Impact of IL-17-producing γδ T cells on chronic otitis media induced by nontypeable Haemophilus influenzae in a mouse model
Abstract Nontypeable Haemophilus influenzae (NTHi) is considered a major pathogen underlying middle ear infection. This study aimed to investigate the impact of IL-17 on chronic otitis media (COM) induced by NTHi in mice. NTHi was inoculated into the tympanic bulla with eustachian tubal obstruction....
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| Veröffentlicht in: | Pathogens and disease 2023-01, Vol.81 |
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| creator | Hirano, Takashi Kawano, Toshiaki Kadowaki, Yoshinori Moriyama, Munehito Umemoto, Shingo Yoshinaga, Kazuhiro Matsunaga, Takayuki Suzuki, Masashi |
| description | Abstract
Nontypeable Haemophilus influenzae (NTHi) is considered a major pathogen underlying middle ear infection. This study aimed to investigate the impact of IL-17 on chronic otitis media (COM) induced by NTHi in mice. NTHi was inoculated into the tympanic bulla with eustachian tubal obstruction. Middle ear effusions (MEEs) and tissues were collected on days 3, 14, and at 1, 2, and 6 months after injection. The expression of interleukin-17A (IL-17A) in MEEs was significantly elevated compared to that in the control group at the translational and transcriptional levels during the experiments. The quantities of IL-17-producing γδ T cells were significantly increased compared to that in the control group during COM, but that of Th17 cells did not. Depletion of γδ T cells by anti-γδ T-cell receptor (TCR) monoclonal antibody (mAb) administration significantly decreased the bacteria counts and the concentrations of IL-1β, IL-6, IL-17A, TNF-α, and IL-10 in MEEs. Our results suggest that IL-17 may play an important role in prolonging the inflammation in the middle ear in COM and that IL-17-producing γδ T cells may contribute to the exacerbated inflammatory response in the middle ear. In this study, anti-γδ TCR mAb administration was found to improve chronic middle ear inflammatory conditions.
IL-17-producing γδ T cells and chronic otitis media. |
| doi_str_mv | 10.1093/femspd/ftad029 |
| format | Article |
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Nontypeable Haemophilus influenzae (NTHi) is considered a major pathogen underlying middle ear infection. This study aimed to investigate the impact of IL-17 on chronic otitis media (COM) induced by NTHi in mice. NTHi was inoculated into the tympanic bulla with eustachian tubal obstruction. Middle ear effusions (MEEs) and tissues were collected on days 3, 14, and at 1, 2, and 6 months after injection. The expression of interleukin-17A (IL-17A) in MEEs was significantly elevated compared to that in the control group at the translational and transcriptional levels during the experiments. The quantities of IL-17-producing γδ T cells were significantly increased compared to that in the control group during COM, but that of Th17 cells did not. Depletion of γδ T cells by anti-γδ T-cell receptor (TCR) monoclonal antibody (mAb) administration significantly decreased the bacteria counts and the concentrations of IL-1β, IL-6, IL-17A, TNF-α, and IL-10 in MEEs. Our results suggest that IL-17 may play an important role in prolonging the inflammation in the middle ear in COM and that IL-17-producing γδ T cells may contribute to the exacerbated inflammatory response in the middle ear. In this study, anti-γδ TCR mAb administration was found to improve chronic middle ear inflammatory conditions.
IL-17-producing γδ T cells and chronic otitis media.</description><identifier>ISSN: 2049-632X</identifier><identifier>EISSN: 2049-632X</identifier><identifier>DOI: 10.1093/femspd/ftad029</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Chronic infection ; Ear diseases ; Haemophilus influenzae ; Helper cells ; Inflammation ; Inflammatory response ; Interleukin 17 ; Lymphocytes ; Lymphocytes T ; Middle ear ; Monoclonal antibodies ; Otitis media ; T cell receptors ; Tumor necrosis factor-α</subject><ispartof>Pathogens and disease, 2023-01, Vol.81</ispartof><rights>The Author(s) 2023. Published by Oxford University Press on behalf of FEMS. 2023</rights><rights>The Author(s) 2023. Published by Oxford University Press on behalf of FEMS.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0001-8579-5065</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1598,27903,27904</link.rule.ids><linktorsrc>$$Uhttps://dx.doi.org/10.1093/femspd/ftad029$$EView_record_in_Oxford_University_Press$$FView_record_in_$$GOxford_University_Press</linktorsrc></links><search><creatorcontrib>Hirano, Takashi</creatorcontrib><creatorcontrib>Kawano, Toshiaki</creatorcontrib><creatorcontrib>Kadowaki, Yoshinori</creatorcontrib><creatorcontrib>Moriyama, Munehito</creatorcontrib><creatorcontrib>Umemoto, Shingo</creatorcontrib><creatorcontrib>Yoshinaga, Kazuhiro</creatorcontrib><creatorcontrib>Matsunaga, Takayuki</creatorcontrib><creatorcontrib>Suzuki, Masashi</creatorcontrib><title>Impact of IL-17-producing γδ T cells on chronic otitis media induced by nontypeable Haemophilus influenzae in a mouse model</title><title>Pathogens and disease</title><description>Abstract
Nontypeable Haemophilus influenzae (NTHi) is considered a major pathogen underlying middle ear infection. This study aimed to investigate the impact of IL-17 on chronic otitis media (COM) induced by NTHi in mice. NTHi was inoculated into the tympanic bulla with eustachian tubal obstruction. Middle ear effusions (MEEs) and tissues were collected on days 3, 14, and at 1, 2, and 6 months after injection. The expression of interleukin-17A (IL-17A) in MEEs was significantly elevated compared to that in the control group at the translational and transcriptional levels during the experiments. The quantities of IL-17-producing γδ T cells were significantly increased compared to that in the control group during COM, but that of Th17 cells did not. Depletion of γδ T cells by anti-γδ T-cell receptor (TCR) monoclonal antibody (mAb) administration significantly decreased the bacteria counts and the concentrations of IL-1β, IL-6, IL-17A, TNF-α, and IL-10 in MEEs. Our results suggest that IL-17 may play an important role in prolonging the inflammation in the middle ear in COM and that IL-17-producing γδ T cells may contribute to the exacerbated inflammatory response in the middle ear. In this study, anti-γδ TCR mAb administration was found to improve chronic middle ear inflammatory conditions.
IL-17-producing γδ T cells and chronic otitis media.</description><subject>Chronic infection</subject><subject>Ear diseases</subject><subject>Haemophilus influenzae</subject><subject>Helper cells</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Interleukin 17</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Middle ear</subject><subject>Monoclonal antibodies</subject><subject>Otitis media</subject><subject>T cell receptors</subject><subject>Tumor necrosis factor-α</subject><issn>2049-632X</issn><issn>2049-632X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkc9KxDAQxoMoKLpXzwEveuhu0rRJcxTxz8KClxW8lTSZaKRNatMeVvCp9Dn2mYysB_HiHGbm8PuGb_gQOqVkTolkCwtd7M3CjsqQXO6ho5wUMuMsf9z_tR-iWYwvJFVV0krwI_S-7HqlRxwsXq4yKrJ-CGbSzj_h7cf2E6-xhraNOHisn4fgncZhdKOLuAPjFHY-0WBws8E--HHTg2pawHcKutA_u3aKCbHtBP5NQVqxwl2YIqRuoD1BB1a1EWY_8xg93Fyvr-6y1f3t8upylWmWyzEraSNyCkZWTcMUM5JTRiqaN0QLKCrDFOeF4Q3PgVthtSFccqVKy0nBCiPYMTrf3U3fvU4Qx7pz8fsx5SG5qfNKCCakLMqEnv1BX8I0-OSuZqQknJa0LBI131F6CDEOYOt-cJ0aNjUl9Xcg9S6Q-ieQJLjYCcLU_8d-ATMVkIQ</recordid><startdate>20230117</startdate><enddate>20230117</enddate><creator>Hirano, Takashi</creator><creator>Kawano, Toshiaki</creator><creator>Kadowaki, Yoshinori</creator><creator>Moriyama, Munehito</creator><creator>Umemoto, Shingo</creator><creator>Yoshinaga, Kazuhiro</creator><creator>Matsunaga, Takayuki</creator><creator>Suzuki, Masashi</creator><general>Oxford University Press</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8579-5065</orcidid></search><sort><creationdate>20230117</creationdate><title>Impact of IL-17-producing γδ T cells on chronic otitis media induced by nontypeable Haemophilus influenzae in a mouse model</title><author>Hirano, Takashi ; Kawano, Toshiaki ; Kadowaki, Yoshinori ; Moriyama, Munehito ; Umemoto, Shingo ; Yoshinaga, Kazuhiro ; Matsunaga, Takayuki ; Suzuki, Masashi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c329t-51b721ed98bb3a3d96130812b0c7e48d3a664d6b62e6f7fcd0696aa5f60434d73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Chronic infection</topic><topic>Ear diseases</topic><topic>Haemophilus influenzae</topic><topic>Helper cells</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Interleukin 17</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Middle ear</topic><topic>Monoclonal antibodies</topic><topic>Otitis media</topic><topic>T cell receptors</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hirano, Takashi</creatorcontrib><creatorcontrib>Kawano, Toshiaki</creatorcontrib><creatorcontrib>Kadowaki, Yoshinori</creatorcontrib><creatorcontrib>Moriyama, Munehito</creatorcontrib><creatorcontrib>Umemoto, Shingo</creatorcontrib><creatorcontrib>Yoshinaga, Kazuhiro</creatorcontrib><creatorcontrib>Matsunaga, Takayuki</creatorcontrib><creatorcontrib>Suzuki, Masashi</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Pathogens and disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Hirano, Takashi</au><au>Kawano, Toshiaki</au><au>Kadowaki, Yoshinori</au><au>Moriyama, Munehito</au><au>Umemoto, Shingo</au><au>Yoshinaga, Kazuhiro</au><au>Matsunaga, Takayuki</au><au>Suzuki, Masashi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of IL-17-producing γδ T cells on chronic otitis media induced by nontypeable Haemophilus influenzae in a mouse model</atitle><jtitle>Pathogens and disease</jtitle><date>2023-01-17</date><risdate>2023</risdate><volume>81</volume><issn>2049-632X</issn><eissn>2049-632X</eissn><abstract>Abstract
Nontypeable Haemophilus influenzae (NTHi) is considered a major pathogen underlying middle ear infection. This study aimed to investigate the impact of IL-17 on chronic otitis media (COM) induced by NTHi in mice. NTHi was inoculated into the tympanic bulla with eustachian tubal obstruction. Middle ear effusions (MEEs) and tissues were collected on days 3, 14, and at 1, 2, and 6 months after injection. The expression of interleukin-17A (IL-17A) in MEEs was significantly elevated compared to that in the control group at the translational and transcriptional levels during the experiments. The quantities of IL-17-producing γδ T cells were significantly increased compared to that in the control group during COM, but that of Th17 cells did not. Depletion of γδ T cells by anti-γδ T-cell receptor (TCR) monoclonal antibody (mAb) administration significantly decreased the bacteria counts and the concentrations of IL-1β, IL-6, IL-17A, TNF-α, and IL-10 in MEEs. Our results suggest that IL-17 may play an important role in prolonging the inflammation in the middle ear in COM and that IL-17-producing γδ T cells may contribute to the exacerbated inflammatory response in the middle ear. In this study, anti-γδ TCR mAb administration was found to improve chronic middle ear inflammatory conditions.
IL-17-producing γδ T cells and chronic otitis media.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><doi>10.1093/femspd/ftad029</doi><orcidid>https://orcid.org/0000-0001-8579-5065</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Chronic infection Ear diseases Haemophilus influenzae Helper cells Inflammation Inflammatory response Interleukin 17 Lymphocytes Lymphocytes T Middle ear Monoclonal antibodies Otitis media T cell receptors Tumor necrosis factor-α |
| title | Impact of IL-17-producing γδ T cells on chronic otitis media induced by nontypeable Haemophilus influenzae in a mouse model |
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