Proinflammatory cytokines and ARDS pulmonary edema fluid induce CD40 on human mesenchymal stromal cells-A potential mechanism for immune modulation
Human mesenchymal stem/stromal cells (hMSCs) are a promising therapy for acute respiratory distress syndrome (ARDS) and other inflammatory conditions. While considerable research has focused on paracrine effects and mitochondrial transfer that improve lung fluid balance, hMSCs are well known to have...
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| description | Human mesenchymal stem/stromal cells (hMSCs) are a promising therapy for acute respiratory distress syndrome (ARDS) and other inflammatory conditions. While considerable research has focused on paracrine effects and mitochondrial transfer that improve lung fluid balance, hMSCs are well known to have immunomodulatory properties as well. Some of these immunomodulatory properties have been related to previously reported paracrine effectors such as indoleamine-2,3-dioxygenase (IDO), but these effects cannot fully account for cell-contact dependent immunomodulation. Here, we report that CD40 is upregulated on hMSCs under the same conditions previously reported to induce IDO. Further, CD40 transcription is also upregulated on hMSCs by ARDS pulmonary edema fluid but not by hydrostatic pulmonary edema fluid. Transcription of CD40, as well as paracrine effectors TSG6 and PTGS2 remained significantly upregulated for at least 12 hours after withdrawal of cytokine stimulation. Finally, induction of this immune phenotype altered the transdifferentiation of hMSCs, one of their hallmark properties. CD40 may play an important role in the immunomodulatory effects of hMSCs in ARDS and inflammation. |
| doi_str_mv | 10.1371/journal.pone.0240319 |
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While considerable research has focused on paracrine effects and mitochondrial transfer that improve lung fluid balance, hMSCs are well known to have immunomodulatory properties as well. Some of these immunomodulatory properties have been related to previously reported paracrine effectors such as indoleamine-2,3-dioxygenase (IDO), but these effects cannot fully account for cell-contact dependent immunomodulation. Here, we report that CD40 is upregulated on hMSCs under the same conditions previously reported to induce IDO. Further, CD40 transcription is also upregulated on hMSCs by ARDS pulmonary edema fluid but not by hydrostatic pulmonary edema fluid. Transcription of CD40, as well as paracrine effectors TSG6 and PTGS2 remained significantly upregulated for at least 12 hours after withdrawal of cytokine stimulation. Finally, induction of this immune phenotype altered the transdifferentiation of hMSCs, one of their hallmark properties. CD40 may play an important role in the immunomodulatory effects of hMSCs in ARDS and inflammation.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0240319</identifier><identifier>PMID: 33021986</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult respiratory distress syndrome ; Biology and Life Sciences ; Bronchoalveolar Lavage Fluid - immunology ; Care and treatment ; CD40 antigen ; CD40 Antigens - genetics ; Cell Adhesion Molecules - genetics ; Cell Transdifferentiation ; Cells, Cultured ; Cloning ; Cyclooxygenase 2 - genetics ; Cytokines ; Cytokines - pharmacology ; Dioxygenase ; Edema ; Effectors ; Experiments ; Female ; Flow cytometry ; Health aspects ; Humans ; Immune response ; Immune system ; Immunomodulation ; Inflammation ; Laboratories ; Lipopolysaccharides - pharmacology ; Male ; Medicine ; Medicine and Health Sciences ; Mesenchymal stem cells ; Mesenchymal Stem Cells - cytology ; Mesenchymal Stem Cells - drug effects ; Mesenchymal Stem Cells - immunology ; Mesenchyme ; Mitochondria ; Neutrophils ; Paracrine signalling ; Phenotypes ; Physiological aspects ; Properties (attributes) ; Pulmonary edema ; R&D ; Research & development ; Research and Analysis Methods ; Respiratory distress syndrome ; Respiratory Distress Syndrome - immunology ; Respiratory Distress Syndrome - therapy ; Sepsis ; Stromal cells ; Transcription ; Transcription, Genetic ; Tumor necrosis factor-TNF ; Up-Regulation</subject><ispartof>PloS one, 2020-10, Vol.15 (10), p.e0240319-e0240319</ispartof><rights>COPYRIGHT 2020 Public Library of Science</rights><rights>2020 Wilfong et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020 Wilfong et al 2020 Wilfong et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-befc569ca1d9e0b93bf68b3a8f06275a84cabfd2caea84e0a14ea855809e78fe3</citedby><cites>FETCH-LOGICAL-c692t-befc569ca1d9e0b93bf68b3a8f06275a84cabfd2caea84e0a14ea855809e78fe3</cites><orcidid>0000-0001-5435-6668 ; 0000-0002-6584-1578</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/PMC7537876/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7537876/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27902,27903,53768,53770,79345,79346</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33021986$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Zhao, You-Yang</contributor><creatorcontrib>Wilfong, Erin M</creatorcontrib><creatorcontrib>Croze, Roxanne</creatorcontrib><creatorcontrib>Fang, Xiaohui</creatorcontrib><creatorcontrib>Schwede, Matthew</creatorcontrib><creatorcontrib>Niemi, Erene</creatorcontrib><creatorcontrib>López, Giselle Y</creatorcontrib><creatorcontrib>Lee, Jae-Woo</creatorcontrib><creatorcontrib>Nakamura, Mary C</creatorcontrib><creatorcontrib>Matthay, Michael A</creatorcontrib><title>Proinflammatory cytokines and ARDS pulmonary edema fluid induce CD40 on human mesenchymal stromal cells-A potential mechanism for immune modulation</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Human mesenchymal stem/stromal cells (hMSCs) are a promising therapy for acute respiratory distress syndrome (ARDS) and other inflammatory conditions. 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While considerable research has focused on paracrine effects and mitochondrial transfer that improve lung fluid balance, hMSCs are well known to have immunomodulatory properties as well. Some of these immunomodulatory properties have been related to previously reported paracrine effectors such as indoleamine-2,3-dioxygenase (IDO), but these effects cannot fully account for cell-contact dependent immunomodulation. Here, we report that CD40 is upregulated on hMSCs under the same conditions previously reported to induce IDO. Further, CD40 transcription is also upregulated on hMSCs by ARDS pulmonary edema fluid but not by hydrostatic pulmonary edema fluid. Transcription of CD40, as well as paracrine effectors TSG6 and PTGS2 remained significantly upregulated for at least 12 hours after withdrawal of cytokine stimulation. Finally, induction of this immune phenotype altered the transdifferentiation of hMSCs, one of their hallmark properties. CD40 may play an important role in the immunomodulatory effects of hMSCs in ARDS and inflammation.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>33021986</pmid><doi>10.1371/journal.pone.0240319</doi><tpages>e0240319</tpages><orcidid>https://orcid.org/0000-0001-5435-6668</orcidid><orcidid>https://orcid.org/0000-0002-6584-1578</orcidid><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2020-10, Vol.15 (10), p.e0240319-e0240319 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2448835634 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Adult respiratory distress syndrome Biology and Life Sciences Bronchoalveolar Lavage Fluid - immunology Care and treatment CD40 antigen CD40 Antigens - genetics Cell Adhesion Molecules - genetics Cell Transdifferentiation Cells, Cultured Cloning Cyclooxygenase 2 - genetics Cytokines Cytokines - pharmacology Dioxygenase Edema Effectors Experiments Female Flow cytometry Health aspects Humans Immune response Immune system Immunomodulation Inflammation Laboratories Lipopolysaccharides - pharmacology Male Medicine Medicine and Health Sciences Mesenchymal stem cells Mesenchymal Stem Cells - cytology Mesenchymal Stem Cells - drug effects Mesenchymal Stem Cells - immunology Mesenchyme Mitochondria Neutrophils Paracrine signalling Phenotypes Physiological aspects Properties (attributes) Pulmonary edema R&D Research & development Research and Analysis Methods Respiratory distress syndrome Respiratory Distress Syndrome - immunology Respiratory Distress Syndrome - therapy Sepsis Stromal cells Transcription Transcription, Genetic Tumor necrosis factor-TNF Up-Regulation |
| title | Proinflammatory cytokines and ARDS pulmonary edema fluid induce CD40 on human mesenchymal stromal cells-A potential mechanism for immune modulation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T08%3A35%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Proinflammatory%20cytokines%20and%20ARDS%20pulmonary%20edema%20fluid%20induce%20CD40%20on%20human%20mesenchymal%20stromal%20cells-A%20potential%20mechanism%20for%20immune%20modulation&rft.jtitle=PloS%20one&rft.au=Wilfong,%20Erin%20M&rft.date=2020-10-06&rft.volume=15&rft.issue=10&rft.spage=e0240319&rft.epage=e0240319&rft.pages=e0240319-e0240319&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0240319&rft_dat=%3Cgale_plos_%3EA637613560%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2448835634&rft_id=info:pmid/33021986&rft_galeid=A637613560&rft_doaj_id=oai_doaj_org_article_33225ae15bf14bf0ae0595fe003a9be8&rfr_iscdi=true |