Theophylline Attenuates BLM-Induced Pulmonary Fibrosis by Inhibiting Th17 Differentiation
Idiopathic pulmonary fibrosis (IPF) is a chronic and refractory interstitial lung disease. Although there are two approved drugs for IPF, they were not able to completely cure the disease. Therefore, the development of new drugs is required for the effective treatment of IPF. In this study, we inves...
Gespeichert in:
| Veröffentlicht in: | International journal of molecular sciences 2023-01, Vol.24 (2), p.1019 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 2 |
| container_start_page | 1019 |
| container_title | International journal of molecular sciences |
| container_volume | 24 |
| creator | Park, Soo-Jin Hahn, Hwa-Jeong Oh, Sei-Ryang Lee, Hyun-Jun |
| description | Idiopathic pulmonary fibrosis (IPF) is a chronic and refractory interstitial lung disease. Although there are two approved drugs for IPF, they were not able to completely cure the disease. Therefore, the development of new drugs is required for the effective treatment of IPF. In this study, we investigated the effect of theophylline, which has long been used for the treatment of asthma, on pulmonary fibrosis. The administration of theophylline attenuated the fibrotic changes of lung tissues and improved mechanical pulmonary functions in bleomycin (BLM)-induced pulmonary fibrosis. Theophylline treatment suppressed IL-17 production through inhibiting cytokines controlling Th17 differentiation; TGF-β, IL-6, IL-1β, and IL-23. The inhibition of IL-6 and IL-1β by theophylline is mediated by suppressing BLM-induced ROS production and NF-κB activation in epithelial cells. We further demonstrated that theophylline inhibited TGF-β-induced epithelial-to-mesenchymal transition in epithelial cells through suppressing the phosphorylation of Smad2/3 and AKT. The inhibitory effects of theophylline on the phosphorylation of Smad2/3 and AKT were recapitulated in BLM-treated lung tissues. Taken together, these results demonstrated that theophylline prevents pulmonary fibrosis by inhibiting Th17 differentiation and TGF-β signaling. |
| doi_str_mv | 10.3390/ijms24021019 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9860752</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2768232973</sourcerecordid><originalsourceid>FETCH-LOGICAL-c412t-e3c5d2da855686121d336a14530b628eb686a0c38a6c4792a0205451f9bf10613</originalsourceid><addsrcrecordid>eNpdkb1PwzAQxS0E4ntjRpFYGAj4I3HiBakUCpWKYCgDk-UkTuMqsYvtIPW_x1VLVZjudPfT07t7AFwgeEsIg3dq3jmcQIwgYnvgGCUYxxDSbH-nPwInzs0hxASn7BAcEUqzJCXkGHxOG2kWzbJtlZbRwHupe-Glix4mr_FYV30pq-i9bzujhV1GI1VY45SLimU01o0qlFd6Fk0blEWPqq6lldor4ZXRZ-CgFq2T55t6Cj5GT9PhSzx5ex4PB5O4TBD2sSRlWuFK5GlKc4owqgihAgV3sKA4l0WYCliSXNAyyRgWEMM0SVHNihpBisgpuF_rLvqik1UZDFjR8oVVXXDMjVD870arhs_MN2c5hVmKg8D1RsCar146zzvlStm2QkvTO44zmofHsYwE9OofOje91eG8FZVhzBCCgbpZU2X4lbOy3ppBkK8y47uZBfxy94At_BsS-QG3ZJHR</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2767229110</pqid></control><display><type>article</type><title>Theophylline Attenuates BLM-Induced Pulmonary Fibrosis by Inhibiting Th17 Differentiation</title><source>MEDLINE</source><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Park, Soo-Jin ; Hahn, Hwa-Jeong ; Oh, Sei-Ryang ; Lee, Hyun-Jun</creator><creatorcontrib>Park, Soo-Jin ; Hahn, Hwa-Jeong ; Oh, Sei-Ryang ; Lee, Hyun-Jun</creatorcontrib><description>Idiopathic pulmonary fibrosis (IPF) is a chronic and refractory interstitial lung disease. Although there are two approved drugs for IPF, they were not able to completely cure the disease. Therefore, the development of new drugs is required for the effective treatment of IPF. In this study, we investigated the effect of theophylline, which has long been used for the treatment of asthma, on pulmonary fibrosis. The administration of theophylline attenuated the fibrotic changes of lung tissues and improved mechanical pulmonary functions in bleomycin (BLM)-induced pulmonary fibrosis. Theophylline treatment suppressed IL-17 production through inhibiting cytokines controlling Th17 differentiation; TGF-β, IL-6, IL-1β, and IL-23. The inhibition of IL-6 and IL-1β by theophylline is mediated by suppressing BLM-induced ROS production and NF-κB activation in epithelial cells. We further demonstrated that theophylline inhibited TGF-β-induced epithelial-to-mesenchymal transition in epithelial cells through suppressing the phosphorylation of Smad2/3 and AKT. The inhibitory effects of theophylline on the phosphorylation of Smad2/3 and AKT were recapitulated in BLM-treated lung tissues. Taken together, these results demonstrated that theophylline prevents pulmonary fibrosis by inhibiting Th17 differentiation and TGF-β signaling.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms24021019</identifier><identifier>PMID: 36674533</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>AKT protein ; Animals ; Bleomycin ; Bleomycin - toxicity ; Cell activation ; Cell Differentiation ; Collagen ; Cytokines ; Differentiation ; Drug development ; Drugs ; Epithelial cells ; Epithelium ; Extracellular matrix ; Fibroblasts ; Fibrosis ; Growth factors ; Helper cells ; Idiopathic Pulmonary Fibrosis - chemically induced ; Idiopathic Pulmonary Fibrosis - drug therapy ; IL-1β ; Interleukin 17 ; Interleukin 23 ; Interleukin 6 ; Interleukin-6 - pharmacology ; Kinases ; Lavage ; Lung ; Lung diseases ; Lymphocytes T ; Mesenchyme ; Mice ; Mice, Inbred C57BL ; NF-κB protein ; Oral administration ; Pathogenesis ; Phosphorylation ; Proteins ; Proto-Oncogene Proteins c-akt ; Pulmonary fibrosis ; Pulmonary functions ; Respiratory system ; Smad2 protein ; Theophylline ; Theophylline - pharmacology ; Transforming Growth Factor beta - pharmacology ; Transforming growth factor-b</subject><ispartof>International journal of molecular sciences, 2023-01, Vol.24 (2), p.1019</ispartof><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 by the authors. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-e3c5d2da855686121d336a14530b628eb686a0c38a6c4792a0205451f9bf10613</citedby><cites>FETCH-LOGICAL-c412t-e3c5d2da855686121d336a14530b628eb686a0c38a6c4792a0205451f9bf10613</cites><orcidid>0000-0002-9769-4779 ; 0000-0003-1293-6159 ; 0000-0002-9304-4840</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9860752/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9860752/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27915,27916,53782,53784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36674533$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Park, Soo-Jin</creatorcontrib><creatorcontrib>Hahn, Hwa-Jeong</creatorcontrib><creatorcontrib>Oh, Sei-Ryang</creatorcontrib><creatorcontrib>Lee, Hyun-Jun</creatorcontrib><title>Theophylline Attenuates BLM-Induced Pulmonary Fibrosis by Inhibiting Th17 Differentiation</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Idiopathic pulmonary fibrosis (IPF) is a chronic and refractory interstitial lung disease. Although there are two approved drugs for IPF, they were not able to completely cure the disease. Therefore, the development of new drugs is required for the effective treatment of IPF. In this study, we investigated the effect of theophylline, which has long been used for the treatment of asthma, on pulmonary fibrosis. The administration of theophylline attenuated the fibrotic changes of lung tissues and improved mechanical pulmonary functions in bleomycin (BLM)-induced pulmonary fibrosis. Theophylline treatment suppressed IL-17 production through inhibiting cytokines controlling Th17 differentiation; TGF-β, IL-6, IL-1β, and IL-23. The inhibition of IL-6 and IL-1β by theophylline is mediated by suppressing BLM-induced ROS production and NF-κB activation in epithelial cells. We further demonstrated that theophylline inhibited TGF-β-induced epithelial-to-mesenchymal transition in epithelial cells through suppressing the phosphorylation of Smad2/3 and AKT. The inhibitory effects of theophylline on the phosphorylation of Smad2/3 and AKT were recapitulated in BLM-treated lung tissues. Taken together, these results demonstrated that theophylline prevents pulmonary fibrosis by inhibiting Th17 differentiation and TGF-β signaling.</description><subject>AKT protein</subject><subject>Animals</subject><subject>Bleomycin</subject><subject>Bleomycin - toxicity</subject><subject>Cell activation</subject><subject>Cell Differentiation</subject><subject>Collagen</subject><subject>Cytokines</subject><subject>Differentiation</subject><subject>Drug development</subject><subject>Drugs</subject><subject>Epithelial cells</subject><subject>Epithelium</subject><subject>Extracellular matrix</subject><subject>Fibroblasts</subject><subject>Fibrosis</subject><subject>Growth factors</subject><subject>Helper cells</subject><subject>Idiopathic Pulmonary Fibrosis - chemically induced</subject><subject>Idiopathic Pulmonary Fibrosis - drug therapy</subject><subject>IL-1β</subject><subject>Interleukin 17</subject><subject>Interleukin 23</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - pharmacology</subject><subject>Kinases</subject><subject>Lavage</subject><subject>Lung</subject><subject>Lung diseases</subject><subject>Lymphocytes T</subject><subject>Mesenchyme</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NF-κB protein</subject><subject>Oral administration</subject><subject>Pathogenesis</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt</subject><subject>Pulmonary fibrosis</subject><subject>Pulmonary functions</subject><subject>Respiratory system</subject><subject>Smad2 protein</subject><subject>Theophylline</subject><subject>Theophylline - pharmacology</subject><subject>Transforming Growth Factor beta - pharmacology</subject><subject>Transforming growth factor-b</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkb1PwzAQxS0E4ntjRpFYGAj4I3HiBakUCpWKYCgDk-UkTuMqsYvtIPW_x1VLVZjudPfT07t7AFwgeEsIg3dq3jmcQIwgYnvgGCUYxxDSbH-nPwInzs0hxASn7BAcEUqzJCXkGHxOG2kWzbJtlZbRwHupe-Glix4mr_FYV30pq-i9bzujhV1GI1VY45SLimU01o0qlFd6Fk0blEWPqq6lldor4ZXRZ-CgFq2T55t6Cj5GT9PhSzx5ex4PB5O4TBD2sSRlWuFK5GlKc4owqgihAgV3sKA4l0WYCliSXNAyyRgWEMM0SVHNihpBisgpuF_rLvqik1UZDFjR8oVVXXDMjVD870arhs_MN2c5hVmKg8D1RsCar146zzvlStm2QkvTO44zmofHsYwE9OofOje91eG8FZVhzBCCgbpZU2X4lbOy3ppBkK8y47uZBfxy94At_BsS-QG3ZJHR</recordid><startdate>20230105</startdate><enddate>20230105</enddate><creator>Park, Soo-Jin</creator><creator>Hahn, Hwa-Jeong</creator><creator>Oh, Sei-Ryang</creator><creator>Lee, Hyun-Jun</creator><general>MDPI AG</general><general>MDPI</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>COVID</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9769-4779</orcidid><orcidid>https://orcid.org/0000-0003-1293-6159</orcidid><orcidid>https://orcid.org/0000-0002-9304-4840</orcidid></search><sort><creationdate>20230105</creationdate><title>Theophylline Attenuates BLM-Induced Pulmonary Fibrosis by Inhibiting Th17 Differentiation</title><author>Park, Soo-Jin ; Hahn, Hwa-Jeong ; Oh, Sei-Ryang ; Lee, Hyun-Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-e3c5d2da855686121d336a14530b628eb686a0c38a6c4792a0205451f9bf10613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>AKT protein</topic><topic>Animals</topic><topic>Bleomycin</topic><topic>Bleomycin - toxicity</topic><topic>Cell activation</topic><topic>Cell Differentiation</topic><topic>Collagen</topic><topic>Cytokines</topic><topic>Differentiation</topic><topic>Drug development</topic><topic>Drugs</topic><topic>Epithelial cells</topic><topic>Epithelium</topic><topic>Extracellular matrix</topic><topic>Fibroblasts</topic><topic>Fibrosis</topic><topic>Growth factors</topic><topic>Helper cells</topic><topic>Idiopathic Pulmonary Fibrosis - chemically induced</topic><topic>Idiopathic Pulmonary Fibrosis - drug therapy</topic><topic>IL-1β</topic><topic>Interleukin 17</topic><topic>Interleukin 23</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - pharmacology</topic><topic>Kinases</topic><topic>Lavage</topic><topic>Lung</topic><topic>Lung diseases</topic><topic>Lymphocytes T</topic><topic>Mesenchyme</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NF-κB protein</topic><topic>Oral administration</topic><topic>Pathogenesis</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt</topic><topic>Pulmonary fibrosis</topic><topic>Pulmonary functions</topic><topic>Respiratory system</topic><topic>Smad2 protein</topic><topic>Theophylline</topic><topic>Theophylline - pharmacology</topic><topic>Transforming Growth Factor beta - pharmacology</topic><topic>Transforming growth factor-b</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Park, Soo-Jin</creatorcontrib><creatorcontrib>Hahn, Hwa-Jeong</creatorcontrib><creatorcontrib>Oh, Sei-Ryang</creatorcontrib><creatorcontrib>Lee, Hyun-Jun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Coronavirus Research Database</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Park, Soo-Jin</au><au>Hahn, Hwa-Jeong</au><au>Oh, Sei-Ryang</au><au>Lee, Hyun-Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Theophylline Attenuates BLM-Induced Pulmonary Fibrosis by Inhibiting Th17 Differentiation</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2023-01-05</date><risdate>2023</risdate><volume>24</volume><issue>2</issue><spage>1019</spage><pages>1019-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Idiopathic pulmonary fibrosis (IPF) is a chronic and refractory interstitial lung disease. Although there are two approved drugs for IPF, they were not able to completely cure the disease. Therefore, the development of new drugs is required for the effective treatment of IPF. In this study, we investigated the effect of theophylline, which has long been used for the treatment of asthma, on pulmonary fibrosis. The administration of theophylline attenuated the fibrotic changes of lung tissues and improved mechanical pulmonary functions in bleomycin (BLM)-induced pulmonary fibrosis. Theophylline treatment suppressed IL-17 production through inhibiting cytokines controlling Th17 differentiation; TGF-β, IL-6, IL-1β, and IL-23. The inhibition of IL-6 and IL-1β by theophylline is mediated by suppressing BLM-induced ROS production and NF-κB activation in epithelial cells. We further demonstrated that theophylline inhibited TGF-β-induced epithelial-to-mesenchymal transition in epithelial cells through suppressing the phosphorylation of Smad2/3 and AKT. The inhibitory effects of theophylline on the phosphorylation of Smad2/3 and AKT were recapitulated in BLM-treated lung tissues. Taken together, these results demonstrated that theophylline prevents pulmonary fibrosis by inhibiting Th17 differentiation and TGF-β signaling.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>36674533</pmid><doi>10.3390/ijms24021019</doi><orcidid>https://orcid.org/0000-0002-9769-4779</orcidid><orcidid>https://orcid.org/0000-0003-1293-6159</orcidid><orcidid>https://orcid.org/0000-0002-9304-4840</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1422-0067 |
| ispartof | International journal of molecular sciences, 2023-01, Vol.24 (2), p.1019 |
| issn | 1422-0067 1661-6596 1422-0067 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9860752 |
| source | MEDLINE; MDPI - Multidisciplinary Digital Publishing Institute; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | AKT protein Animals Bleomycin Bleomycin - toxicity Cell activation Cell Differentiation Collagen Cytokines Differentiation Drug development Drugs Epithelial cells Epithelium Extracellular matrix Fibroblasts Fibrosis Growth factors Helper cells Idiopathic Pulmonary Fibrosis - chemically induced Idiopathic Pulmonary Fibrosis - drug therapy IL-1β Interleukin 17 Interleukin 23 Interleukin 6 Interleukin-6 - pharmacology Kinases Lavage Lung Lung diseases Lymphocytes T Mesenchyme Mice Mice, Inbred C57BL NF-κB protein Oral administration Pathogenesis Phosphorylation Proteins Proto-Oncogene Proteins c-akt Pulmonary fibrosis Pulmonary functions Respiratory system Smad2 protein Theophylline Theophylline - pharmacology Transforming Growth Factor beta - pharmacology Transforming growth factor-b |
| title | Theophylline Attenuates BLM-Induced Pulmonary Fibrosis by Inhibiting Th17 Differentiation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-15T00%3A54%3A19IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Theophylline%20Attenuates%20BLM-Induced%20Pulmonary%20Fibrosis%20by%20Inhibiting%20Th17%20Differentiation&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Park,%20Soo-Jin&rft.date=2023-01-05&rft.volume=24&rft.issue=2&rft.spage=1019&rft.pages=1019-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms24021019&rft_dat=%3Cproquest_pubme%3E2768232973%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2767229110&rft_id=info:pmid/36674533&rfr_iscdi=true |