Opsonophagocytosis of Chlamydia pneumoniae by Human Monocytes and Neutrophils
The human respiratory tract pathogen , which causes mild to severe infections, has been associated with the development of chronic inflammatory diseases. To understand the biology of infections, several studies have investigated the interaction between and professional phagocytes. However, these stu...
Gespeichert in:
| Veröffentlicht in: | Infection and immunity 2020-06, Vol.88 (7) |
|---|---|
| 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 | 7 |
| container_start_page | |
| container_title | Infection and immunity |
| container_volume | 88 |
| creator | Lausen, Mads Pedersen, Mathilde Selmar Rahman, Nareen Sherzad Kader Holm-Nielsen, Liv Therese Farah, Faduma Yahya Mohamed Christiansen, Gunna Birkelund, Svend |
| description | The human respiratory tract pathogen
, which causes mild to severe infections, has been associated with the development of chronic inflammatory diseases. To understand the biology of
infections, several studies have investigated the interaction between
and professional phagocytes. However, these studies have been conducted under nonopsonizing conditions, making the role of opsonization in
infections elusive. Thus, we analyzed complement and antibody opsonization of
and evaluated how opsonization affects chlamydial infectivity and phagocytosis in human monocytes and neutrophils. We demonstrated that IgG antibodies and activation products of complement C3 and C4 are deposited on the surface of
elementary bodies when incubated in human serum. Complement activation limits
infectivity
and has the potential to induce bacterial lysis by the formation of the membrane attack complex. Coculture of
and freshly isolated human leukocytes showed that complement opsonization is superior to IgG opsonization for efficient opsonophagocytosis of
in monocytes and neutrophils. Neutrophil-mediated phagocytosis of
was crucially dependent on opsonization, while monocytes retained minor phagocytic potential under nonopsonizing conditions. Complement opsonization significantly enhanced the intracellular neutralization of
in peripheral blood mononuclear cells and neutrophils and almost abrogated the infectious potential of
In conclusion, we demonstrated that complements limit
infection
by interfering with
entry into permissive cells by direct complement-induced lysis and by tagging bacteria for efficient phagocytosis in both monocytes and neutrophils. |
| doi_str_mv | 10.1128/IAI.00087-20 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7309617</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2389693696</sourcerecordid><originalsourceid>FETCH-LOGICAL-c384t-bccef1318e07780777a592a0349793bc376a6b6274e2e5305e9569877b7812f83</originalsourceid><addsrcrecordid>eNpVkTtPwzAUhS0EoqWwMaOMDKT4kfixIFUV0EotXWC2HNdpjRI7xAlS_z2GlgoG68q63z33cQC4RnCMEOb388l8DCHkLMXwBAwRFDzNc4xPwRBCJFKRUzYAFyG8x2-WZfwcDAjGPCMMD8Fy1QTvfLNVG693nQ82JL5MpttK1bu1VUnjTF97Z5VJil0y62vlkmWsiLAJiXLr5MX0XRsVbBUuwVmpqmCuDnEE3p4eX6ezdLF6nk8ni1QTnnVpobUpEUHcQMZ4fEzlAitIMsEEKTRhVNGCYpYZbHICcxOXEJyxgnGES05G4GGv2_RFbdbauK5VlWxaW6t2J72y8n_G2a3c-E_JCBQUsShwexBo_UdvQidrG7SpKuWM74PEhAsqCBU0ond7VLc-hNaUxzYIym8HZHRA_jggMYz4zd_RjvDvyckX4zaBwg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2389693696</pqid></control><display><type>article</type><title>Opsonophagocytosis of Chlamydia pneumoniae by Human Monocytes and Neutrophils</title><source>American Society for Microbiology</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Lausen, Mads ; Pedersen, Mathilde Selmar ; Rahman, Nareen Sherzad Kader ; Holm-Nielsen, Liv Therese ; Farah, Faduma Yahya Mohamed ; Christiansen, Gunna ; Birkelund, Svend</creator><contributor>Roy, Craig R.</contributor><creatorcontrib>Lausen, Mads ; Pedersen, Mathilde Selmar ; Rahman, Nareen Sherzad Kader ; Holm-Nielsen, Liv Therese ; Farah, Faduma Yahya Mohamed ; Christiansen, Gunna ; Birkelund, Svend ; Roy, Craig R.</creatorcontrib><description>The human respiratory tract pathogen
, which causes mild to severe infections, has been associated with the development of chronic inflammatory diseases. To understand the biology of
infections, several studies have investigated the interaction between
and professional phagocytes. However, these studies have been conducted under nonopsonizing conditions, making the role of opsonization in
infections elusive. Thus, we analyzed complement and antibody opsonization of
and evaluated how opsonization affects chlamydial infectivity and phagocytosis in human monocytes and neutrophils. We demonstrated that IgG antibodies and activation products of complement C3 and C4 are deposited on the surface of
elementary bodies when incubated in human serum. Complement activation limits
infectivity
and has the potential to induce bacterial lysis by the formation of the membrane attack complex. Coculture of
and freshly isolated human leukocytes showed that complement opsonization is superior to IgG opsonization for efficient opsonophagocytosis of
in monocytes and neutrophils. Neutrophil-mediated phagocytosis of
was crucially dependent on opsonization, while monocytes retained minor phagocytic potential under nonopsonizing conditions. Complement opsonization significantly enhanced the intracellular neutralization of
in peripheral blood mononuclear cells and neutrophils and almost abrogated the infectious potential of
In conclusion, we demonstrated that complements limit
infection
by interfering with
entry into permissive cells by direct complement-induced lysis and by tagging bacteria for efficient phagocytosis in both monocytes and neutrophils.</description><identifier>ISSN: 0019-9567</identifier><identifier>EISSN: 1098-5522</identifier><identifier>DOI: 10.1128/IAI.00087-20</identifier><identifier>PMID: 32284372</identifier><language>eng</language><publisher>United States: American Society for Microbiology</publisher><subject>Antibodies, Bacterial - immunology ; Cellular Microbiology: Pathogen-Host Cell Molecular Interactions ; Chlamydophila Infections - immunology ; Chlamydophila Infections - microbiology ; Chlamydophila pneumoniae - physiology ; Complement Activation - immunology ; Complement System Proteins - immunology ; Complement System Proteins - metabolism ; Humans ; Monocytes - immunology ; Monocytes - metabolism ; Neutrophils - immunology ; Neutrophils - metabolism ; Phagocytosis</subject><ispartof>Infection and immunity, 2020-06, Vol.88 (7)</ispartof><rights>Copyright © 2020 American Society for Microbiology.</rights><rights>Copyright © 2020 American Society for Microbiology. 2020 American Society for Microbiology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c384t-bccef1318e07780777a592a0349793bc376a6b6274e2e5305e9569877b7812f83</citedby><cites>FETCH-LOGICAL-c384t-bccef1318e07780777a592a0349793bc376a6b6274e2e5305e9569877b7812f83</cites><orcidid>0000-0003-2328-5902</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/PMC7309617/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7309617/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,3187,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32284372$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Roy, Craig R.</contributor><creatorcontrib>Lausen, Mads</creatorcontrib><creatorcontrib>Pedersen, Mathilde Selmar</creatorcontrib><creatorcontrib>Rahman, Nareen Sherzad Kader</creatorcontrib><creatorcontrib>Holm-Nielsen, Liv Therese</creatorcontrib><creatorcontrib>Farah, Faduma Yahya Mohamed</creatorcontrib><creatorcontrib>Christiansen, Gunna</creatorcontrib><creatorcontrib>Birkelund, Svend</creatorcontrib><title>Opsonophagocytosis of Chlamydia pneumoniae by Human Monocytes and Neutrophils</title><title>Infection and immunity</title><addtitle>Infect Immun</addtitle><description>The human respiratory tract pathogen
, which causes mild to severe infections, has been associated with the development of chronic inflammatory diseases. To understand the biology of
infections, several studies have investigated the interaction between
and professional phagocytes. However, these studies have been conducted under nonopsonizing conditions, making the role of opsonization in
infections elusive. Thus, we analyzed complement and antibody opsonization of
and evaluated how opsonization affects chlamydial infectivity and phagocytosis in human monocytes and neutrophils. We demonstrated that IgG antibodies and activation products of complement C3 and C4 are deposited on the surface of
elementary bodies when incubated in human serum. Complement activation limits
infectivity
and has the potential to induce bacterial lysis by the formation of the membrane attack complex. Coculture of
and freshly isolated human leukocytes showed that complement opsonization is superior to IgG opsonization for efficient opsonophagocytosis of
in monocytes and neutrophils. Neutrophil-mediated phagocytosis of
was crucially dependent on opsonization, while monocytes retained minor phagocytic potential under nonopsonizing conditions. Complement opsonization significantly enhanced the intracellular neutralization of
in peripheral blood mononuclear cells and neutrophils and almost abrogated the infectious potential of
In conclusion, we demonstrated that complements limit
infection
by interfering with
entry into permissive cells by direct complement-induced lysis and by tagging bacteria for efficient phagocytosis in both monocytes and neutrophils.</description><subject>Antibodies, Bacterial - immunology</subject><subject>Cellular Microbiology: Pathogen-Host Cell Molecular Interactions</subject><subject>Chlamydophila Infections - immunology</subject><subject>Chlamydophila Infections - microbiology</subject><subject>Chlamydophila pneumoniae - physiology</subject><subject>Complement Activation - immunology</subject><subject>Complement System Proteins - immunology</subject><subject>Complement System Proteins - metabolism</subject><subject>Humans</subject><subject>Monocytes - immunology</subject><subject>Monocytes - metabolism</subject><subject>Neutrophils - immunology</subject><subject>Neutrophils - metabolism</subject><subject>Phagocytosis</subject><issn>0019-9567</issn><issn>1098-5522</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkTtPwzAUhS0EoqWwMaOMDKT4kfixIFUV0EotXWC2HNdpjRI7xAlS_z2GlgoG68q63z33cQC4RnCMEOb388l8DCHkLMXwBAwRFDzNc4xPwRBCJFKRUzYAFyG8x2-WZfwcDAjGPCMMD8Fy1QTvfLNVG693nQ82JL5MpttK1bu1VUnjTF97Z5VJil0y62vlkmWsiLAJiXLr5MX0XRsVbBUuwVmpqmCuDnEE3p4eX6ezdLF6nk8ni1QTnnVpobUpEUHcQMZ4fEzlAitIMsEEKTRhVNGCYpYZbHICcxOXEJyxgnGES05G4GGv2_RFbdbauK5VlWxaW6t2J72y8n_G2a3c-E_JCBQUsShwexBo_UdvQidrG7SpKuWM74PEhAsqCBU0ond7VLc-hNaUxzYIym8HZHRA_jggMYz4zd_RjvDvyckX4zaBwg</recordid><startdate>20200622</startdate><enddate>20200622</enddate><creator>Lausen, Mads</creator><creator>Pedersen, Mathilde Selmar</creator><creator>Rahman, Nareen Sherzad Kader</creator><creator>Holm-Nielsen, Liv Therese</creator><creator>Farah, Faduma Yahya Mohamed</creator><creator>Christiansen, Gunna</creator><creator>Birkelund, Svend</creator><general>American Society for Microbiology</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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2328-5902</orcidid></search><sort><creationdate>20200622</creationdate><title>Opsonophagocytosis of Chlamydia pneumoniae by Human Monocytes and Neutrophils</title><author>Lausen, Mads ; Pedersen, Mathilde Selmar ; Rahman, Nareen Sherzad Kader ; Holm-Nielsen, Liv Therese ; Farah, Faduma Yahya Mohamed ; Christiansen, Gunna ; Birkelund, Svend</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c384t-bccef1318e07780777a592a0349793bc376a6b6274e2e5305e9569877b7812f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Antibodies, Bacterial - immunology</topic><topic>Cellular Microbiology: Pathogen-Host Cell Molecular Interactions</topic><topic>Chlamydophila Infections - immunology</topic><topic>Chlamydophila Infections - microbiology</topic><topic>Chlamydophila pneumoniae - physiology</topic><topic>Complement Activation - immunology</topic><topic>Complement System Proteins - immunology</topic><topic>Complement System Proteins - metabolism</topic><topic>Humans</topic><topic>Monocytes - immunology</topic><topic>Monocytes - metabolism</topic><topic>Neutrophils - immunology</topic><topic>Neutrophils - metabolism</topic><topic>Phagocytosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lausen, Mads</creatorcontrib><creatorcontrib>Pedersen, Mathilde Selmar</creatorcontrib><creatorcontrib>Rahman, Nareen Sherzad Kader</creatorcontrib><creatorcontrib>Holm-Nielsen, Liv Therese</creatorcontrib><creatorcontrib>Farah, Faduma Yahya Mohamed</creatorcontrib><creatorcontrib>Christiansen, Gunna</creatorcontrib><creatorcontrib>Birkelund, Svend</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Infection and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lausen, Mads</au><au>Pedersen, Mathilde Selmar</au><au>Rahman, Nareen Sherzad Kader</au><au>Holm-Nielsen, Liv Therese</au><au>Farah, Faduma Yahya Mohamed</au><au>Christiansen, Gunna</au><au>Birkelund, Svend</au><au>Roy, Craig R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Opsonophagocytosis of Chlamydia pneumoniae by Human Monocytes and Neutrophils</atitle><jtitle>Infection and immunity</jtitle><addtitle>Infect Immun</addtitle><date>2020-06-22</date><risdate>2020</risdate><volume>88</volume><issue>7</issue><issn>0019-9567</issn><eissn>1098-5522</eissn><abstract>The human respiratory tract pathogen
, which causes mild to severe infections, has been associated with the development of chronic inflammatory diseases. To understand the biology of
infections, several studies have investigated the interaction between
and professional phagocytes. However, these studies have been conducted under nonopsonizing conditions, making the role of opsonization in
infections elusive. Thus, we analyzed complement and antibody opsonization of
and evaluated how opsonization affects chlamydial infectivity and phagocytosis in human monocytes and neutrophils. We demonstrated that IgG antibodies and activation products of complement C3 and C4 are deposited on the surface of
elementary bodies when incubated in human serum. Complement activation limits
infectivity
and has the potential to induce bacterial lysis by the formation of the membrane attack complex. Coculture of
and freshly isolated human leukocytes showed that complement opsonization is superior to IgG opsonization for efficient opsonophagocytosis of
in monocytes and neutrophils. Neutrophil-mediated phagocytosis of
was crucially dependent on opsonization, while monocytes retained minor phagocytic potential under nonopsonizing conditions. Complement opsonization significantly enhanced the intracellular neutralization of
in peripheral blood mononuclear cells and neutrophils and almost abrogated the infectious potential of
In conclusion, we demonstrated that complements limit
infection
by interfering with
entry into permissive cells by direct complement-induced lysis and by tagging bacteria for efficient phagocytosis in both monocytes and neutrophils.</abstract><cop>United States</cop><pub>American Society for Microbiology</pub><pmid>32284372</pmid><doi>10.1128/IAI.00087-20</doi><orcidid>https://orcid.org/0000-0003-2328-5902</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0019-9567 |
| ispartof | Infection and immunity, 2020-06, Vol.88 (7) |
| issn | 0019-9567 1098-5522 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7309617 |
| source | American Society for Microbiology; MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Antibodies, Bacterial - immunology Cellular Microbiology: Pathogen-Host Cell Molecular Interactions Chlamydophila Infections - immunology Chlamydophila Infections - microbiology Chlamydophila pneumoniae - physiology Complement Activation - immunology Complement System Proteins - immunology Complement System Proteins - metabolism Humans Monocytes - immunology Monocytes - metabolism Neutrophils - immunology Neutrophils - metabolism Phagocytosis |
| title | Opsonophagocytosis of Chlamydia pneumoniae by Human Monocytes and Neutrophils |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-09T04%3A15%3A44IST&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=Opsonophagocytosis%20of%20Chlamydia%20pneumoniae%20by%20Human%20Monocytes%20and%20Neutrophils&rft.jtitle=Infection%20and%20immunity&rft.au=Lausen,%20Mads&rft.date=2020-06-22&rft.volume=88&rft.issue=7&rft.issn=0019-9567&rft.eissn=1098-5522&rft_id=info:doi/10.1128/IAI.00087-20&rft_dat=%3Cproquest_pubme%3E2389693696%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=2389693696&rft_id=info:pmid/32284372&rfr_iscdi=true |