Modulation of the E-cadherin in human cells infected in vitro with Coxiella burnetii
High concentration of soluble E-cadherin (E-cad) was previously found in sera from Q fever patients. Here, BeWo cells which express a high concentration of E-cad were used as an in vitro model to investigate the expression and function of E-cad in response to infection by Coxiella burnetii, the etio...
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| creator | Omar Osman, Ikram Mezouar, Soraya Brahim-Belhaouari, Djamal Mege, Jean-Louis Devaux, Christian Albert |
| description | High concentration of soluble E-cadherin (E-cad) was previously found in sera from Q fever patients. Here, BeWo cells which express a high concentration of E-cad were used as an in vitro model to investigate the expression and function of E-cad in response to infection by Coxiella burnetii, the etiological agent of Q fever. Infection of BeWo cells with C. burnetii leads to a decrease in the number of BeWo cells expressing E-cad at their membrane. A shedding of soluble E-cad was associated with the post-infection decrease of membrane-bound E-cad. The modulation of E-cad expression requires bacterial viability and was not found with heat-inactivated C. burnetii. Moreover, the intracytoplasmic cell concentration of β-catenin (β-cat), a ligand of E-cad, was reduced after bacterial infection, suggesting that the bacterium induces modulation of the E-cad/β-cat signaling pathway and CDH1 and CTNNB1 genes transcription. Finally, several genes operating the canonical Wnt-Frizzled/β-cat pathway were overexpressed in cells infected with C. burnetii. This was particularly evident with the highly virulent strain of C. burnetii, Guiana. Our data demonstrate that infection of BeWo cells by live C. burnetii modulates the E-cad/β-cat signaling pathway. |
| doi_str_mv | 10.1371/journal.pone.0285577 |
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Here, BeWo cells which express a high concentration of E-cad were used as an in vitro model to investigate the expression and function of E-cad in response to infection by Coxiella burnetii, the etiological agent of Q fever. Infection of BeWo cells with C. burnetii leads to a decrease in the number of BeWo cells expressing E-cad at their membrane. A shedding of soluble E-cad was associated with the post-infection decrease of membrane-bound E-cad. The modulation of E-cad expression requires bacterial viability and was not found with heat-inactivated C. burnetii. Moreover, the intracytoplasmic cell concentration of β-catenin (β-cat), a ligand of E-cad, was reduced after bacterial infection, suggesting that the bacterium induces modulation of the E-cad/β-cat signaling pathway and CDH1 and CTNNB1 genes transcription. Finally, several genes operating the canonical Wnt-Frizzled/β-cat pathway were overexpressed in cells infected with C. burnetii. This was particularly evident with the highly virulent strain of C. burnetii, Guiana. Our data demonstrate that infection of BeWo cells by live C. burnetii modulates the E-cad/β-cat signaling pathway.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0285577</identifier><identifier>PMID: 37285354</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Bacteria ; Bacterial diseases ; Bacteriology ; Biology and Life Sciences ; Blood & organ donations ; Cadherins - genetics ; Cadherins - metabolism ; Cardiology and cardiovascular system ; Care and treatment ; Cell division ; Coxiella burnetii ; Cytokines ; Diagnosis ; E-cadherin ; Effectiveness ; Emerging diseases ; Endocarditis ; Fever ; Frizzled protein ; Genes ; Human health and pathology ; Humans ; Infections ; Infectious diseases ; Leukemia ; Life Sciences ; Lymphoma ; Medicine and Health Sciences ; Membranes ; Microbiology and Parasitology ; Modulation ; Parasitology ; Q fever ; Q Fever - microbiology ; Research and Analysis Methods ; Rickettsia ; Risk factors ; Signal transduction ; Signaling ; Software ; Virology ; Virulence ; Wnt protein ; Zoonoses ; β-Catenin</subject><ispartof>PloS one, 2023-06, Vol.18 (6), p.e0285577</ispartof><rights>Copyright: © 2023 Omar Osman et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</rights><rights>COPYRIGHT 2023 Public Library of Science</rights><rights>2023 Omar Osman 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>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>2023 Omar Osman et al 2023 Omar Osman et al</rights><rights>2023 Omar Osman 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c676t-b2156ee709b877ceb6cbd6ce705606830d5aeeae872f496fd54898485c5582b23</cites><orcidid>0000-0001-5141-5298 ; 0000-0002-1112-9921 ; 0000-0002-2285-7051</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/PMC10246793/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10246793/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23871,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37285354$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://amu.hal.science/hal-04125807$$DView record in HAL$$Hfree_for_read</backlink></links><search><contributor>Xing, Li</contributor><creatorcontrib>Omar Osman, Ikram</creatorcontrib><creatorcontrib>Mezouar, Soraya</creatorcontrib><creatorcontrib>Brahim-Belhaouari, Djamal</creatorcontrib><creatorcontrib>Mege, Jean-Louis</creatorcontrib><creatorcontrib>Devaux, Christian Albert</creatorcontrib><title>Modulation of the E-cadherin in human cells infected in vitro with Coxiella burnetii</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>High concentration of soluble E-cadherin (E-cad) was previously found in sera from Q fever patients. Here, BeWo cells which express a high concentration of E-cad were used as an in vitro model to investigate the expression and function of E-cad in response to infection by Coxiella burnetii, the etiological agent of Q fever. Infection of BeWo cells with C. burnetii leads to a decrease in the number of BeWo cells expressing E-cad at their membrane. A shedding of soluble E-cad was associated with the post-infection decrease of membrane-bound E-cad. The modulation of E-cad expression requires bacterial viability and was not found with heat-inactivated C. burnetii. Moreover, the intracytoplasmic cell concentration of β-catenin (β-cat), a ligand of E-cad, was reduced after bacterial infection, suggesting that the bacterium induces modulation of the E-cad/β-cat signaling pathway and CDH1 and CTNNB1 genes transcription. Finally, several genes operating the canonical Wnt-Frizzled/β-cat pathway were overexpressed in cells infected with C. burnetii. This was particularly evident with the highly virulent strain of C. burnetii, Guiana. Our data demonstrate that infection of BeWo cells by live C. burnetii modulates the E-cad/β-cat signaling pathway.</description><subject>Bacteria</subject><subject>Bacterial diseases</subject><subject>Bacteriology</subject><subject>Biology and Life Sciences</subject><subject>Blood & organ donations</subject><subject>Cadherins - genetics</subject><subject>Cadherins - metabolism</subject><subject>Cardiology and cardiovascular system</subject><subject>Care and treatment</subject><subject>Cell division</subject><subject>Coxiella burnetii</subject><subject>Cytokines</subject><subject>Diagnosis</subject><subject>E-cadherin</subject><subject>Effectiveness</subject><subject>Emerging diseases</subject><subject>Endocarditis</subject><subject>Fever</subject><subject>Frizzled protein</subject><subject>Genes</subject><subject>Human health and pathology</subject><subject>Humans</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Leukemia</subject><subject>Life Sciences</subject><subject>Lymphoma</subject><subject>Medicine and Health Sciences</subject><subject>Membranes</subject><subject>Microbiology and Parasitology</subject><subject>Modulation</subject><subject>Parasitology</subject><subject>Q fever</subject><subject>Q Fever - 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Here, BeWo cells which express a high concentration of E-cad were used as an in vitro model to investigate the expression and function of E-cad in response to infection by Coxiella burnetii, the etiological agent of Q fever. Infection of BeWo cells with C. burnetii leads to a decrease in the number of BeWo cells expressing E-cad at their membrane. A shedding of soluble E-cad was associated with the post-infection decrease of membrane-bound E-cad. The modulation of E-cad expression requires bacterial viability and was not found with heat-inactivated C. burnetii. Moreover, the intracytoplasmic cell concentration of β-catenin (β-cat), a ligand of E-cad, was reduced after bacterial infection, suggesting that the bacterium induces modulation of the E-cad/β-cat signaling pathway and CDH1 and CTNNB1 genes transcription. Finally, several genes operating the canonical Wnt-Frizzled/β-cat pathway were overexpressed in cells infected with C. burnetii. This was particularly evident with the highly virulent strain of C. burnetii, Guiana. Our data demonstrate that infection of BeWo cells by live C. burnetii modulates the E-cad/β-cat signaling pathway.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>37285354</pmid><doi>10.1371/journal.pone.0285577</doi><tpages>e0285577</tpages><orcidid>https://orcid.org/0000-0001-5141-5298</orcidid><orcidid>https://orcid.org/0000-0002-1112-9921</orcidid><orcidid>https://orcid.org/0000-0002-2285-7051</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2023-06, Vol.18 (6), p.e0285577 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2823477428 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS) Journals Open Access; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Bacteria Bacterial diseases Bacteriology Biology and Life Sciences Blood & organ donations Cadherins - genetics Cadherins - metabolism Cardiology and cardiovascular system Care and treatment Cell division Coxiella burnetii Cytokines Diagnosis E-cadherin Effectiveness Emerging diseases Endocarditis Fever Frizzled protein Genes Human health and pathology Humans Infections Infectious diseases Leukemia Life Sciences Lymphoma Medicine and Health Sciences Membranes Microbiology and Parasitology Modulation Parasitology Q fever Q Fever - microbiology Research and Analysis Methods Rickettsia Risk factors Signal transduction Signaling Software Virology Virulence Wnt protein Zoonoses β-Catenin |
| title | Modulation of the E-cadherin in human cells infected in vitro with Coxiella burnetii |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-12T08%3A29%3A03IST&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=Modulation%20of%20the%20E-cadherin%20in%20human%20cells%20infected%20in%20vitro%20with%20Coxiella%20burnetii&rft.jtitle=PloS%20one&rft.au=Omar%20Osman,%20Ikram&rft.date=2023-06-07&rft.volume=18&rft.issue=6&rft.spage=e0285577&rft.pages=e0285577-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0285577&rft_dat=%3Cgale_plos_%3EA752130946%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=2823477428&rft_id=info:pmid/37285354&rft_galeid=A752130946&rft_doaj_id=oai_doaj_org_article_e708ce8d476a402fb3d8a18f05ca9152&rfr_iscdi=true |