Neutrophils Are Central to Antibody-Mediated Protection against Genital Chlamydia
Determining the effector populations involved in humoral protection against genital chlamydia infection is crucial to development of an effective chlamydial vaccine. Antibody has been implicated in protection studies in multiple animal models, and we previously showed that the passive transfer of im...
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Veröffentlicht in: | Infection and immunity 2017-10, Vol.85 (10) |
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creator | Naglak, Elizabeth K Morrison, Sandra G Morrison, Richard P |
description | Determining the effector populations involved in humoral protection against genital chlamydia infection is crucial to development of an effective chlamydial vaccine. Antibody has been implicated in protection studies in multiple animal models, and we previously showed that the passive transfer of immune serum alone does not confer immunity in the mouse. Using the
model of genital infection, we demonstrate a protective role for both
-specific immunoglobulin G (IgG) and polymorphonuclear neutrophils and show the importance of an antibody/effector cell interaction in mediating humoral immunity. While neutrophils were found to contribute significantly to antibody-mediated protection
, natural killer (NK) cells were dispensable for protective immunity. Furthermore, gamma interferon (IFN-γ)-stimulated primary peritoneal neutrophils (PPNs) killed chlamydiae
in an antibody-dependent manner. The results from this study support the view that an IFN-γ-activated effector cell population cooperates with antibody to protect against genital chlamydia and establish neutrophils as a key effector cell in this response. |
doi_str_mv | 10.1128/IAI.00409-17 |
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model of genital infection, we demonstrate a protective role for both
-specific immunoglobulin G (IgG) and polymorphonuclear neutrophils and show the importance of an antibody/effector cell interaction in mediating humoral immunity. While neutrophils were found to contribute significantly to antibody-mediated protection
, natural killer (NK) cells were dispensable for protective immunity. Furthermore, gamma interferon (IFN-γ)-stimulated primary peritoneal neutrophils (PPNs) killed chlamydiae
in an antibody-dependent manner. The results from this study support the view that an IFN-γ-activated effector cell population cooperates with antibody to protect against genital chlamydia and establish neutrophils as a key effector cell in this response.</description><identifier>ISSN: 0019-9567</identifier><identifier>EISSN: 1098-5522</identifier><identifier>DOI: 10.1128/IAI.00409-17</identifier><identifier>PMID: 28739831</identifier><language>eng</language><publisher>United States: American Society for Microbiology</publisher><subject>Animals ; Antibodies, Bacterial - blood ; Antibodies, Bacterial - immunology ; CD4-Positive T-Lymphocytes - immunology ; Chlamydia Infections - immunology ; Chlamydia Infections - prevention & control ; Chlamydia muridarum - immunology ; Female ; Genital Diseases, Female - immunology ; Genital Diseases, Female - prevention & control ; Genitalia - immunology ; Genitalia - microbiology ; Immunity, Humoral ; Immunoglobulin G - blood ; Immunoglobulin G - immunology ; Interferon-gamma - immunology ; Interferon-gamma - pharmacology ; Killer Cells, Natural - immunology ; Mice ; Microbial Immunity and Vaccines ; Neutrophils - drug effects ; Neutrophils - immunology ; Sexually Transmitted Diseases - immunology ; Sexually Transmitted Diseases - microbiology ; Sexually Transmitted Diseases - prevention & control</subject><ispartof>Infection and immunity, 2017-10, Vol.85 (10)</ispartof><rights>Copyright © 2017 Naglak et al.</rights><rights>Copyright © 2017 Naglak et al. 2017 Naglak et al.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c380t-58be448de27d342c4afefc0e17ec510b94eaeb6585a7dccb25d98266f76291023</citedby><cites>FETCH-LOGICAL-c380t-58be448de27d342c4afefc0e17ec510b94eaeb6585a7dccb25d98266f76291023</cites><orcidid>0000-0002-9747-9884</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/PMC5607418/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5607418/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,3187,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28739831$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Palmer, Guy H.</contributor><creatorcontrib>Naglak, Elizabeth K</creatorcontrib><creatorcontrib>Morrison, Sandra G</creatorcontrib><creatorcontrib>Morrison, Richard P</creatorcontrib><title>Neutrophils Are Central to Antibody-Mediated Protection against Genital Chlamydia</title><title>Infection and immunity</title><addtitle>Infect Immun</addtitle><description>Determining the effector populations involved in humoral protection against genital chlamydia infection is crucial to development of an effective chlamydial vaccine. Antibody has been implicated in protection studies in multiple animal models, and we previously showed that the passive transfer of immune serum alone does not confer immunity in the mouse. Using the
model of genital infection, we demonstrate a protective role for both
-specific immunoglobulin G (IgG) and polymorphonuclear neutrophils and show the importance of an antibody/effector cell interaction in mediating humoral immunity. While neutrophils were found to contribute significantly to antibody-mediated protection
, natural killer (NK) cells were dispensable for protective immunity. Furthermore, gamma interferon (IFN-γ)-stimulated primary peritoneal neutrophils (PPNs) killed chlamydiae
in an antibody-dependent manner. The results from this study support the view that an IFN-γ-activated effector cell population cooperates with antibody to protect against genital chlamydia and establish neutrophils as a key effector cell in this response.</description><subject>Animals</subject><subject>Antibodies, Bacterial - blood</subject><subject>Antibodies, Bacterial - immunology</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>Chlamydia Infections - immunology</subject><subject>Chlamydia Infections - prevention & control</subject><subject>Chlamydia muridarum - immunology</subject><subject>Female</subject><subject>Genital Diseases, Female - immunology</subject><subject>Genital Diseases, Female - prevention & control</subject><subject>Genitalia - immunology</subject><subject>Genitalia - microbiology</subject><subject>Immunity, Humoral</subject><subject>Immunoglobulin G - blood</subject><subject>Immunoglobulin G - immunology</subject><subject>Interferon-gamma - immunology</subject><subject>Interferon-gamma - pharmacology</subject><subject>Killer Cells, Natural - immunology</subject><subject>Mice</subject><subject>Microbial Immunity and Vaccines</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - immunology</subject><subject>Sexually Transmitted Diseases - immunology</subject><subject>Sexually Transmitted Diseases - microbiology</subject><subject>Sexually Transmitted Diseases - prevention & control</subject><issn>0019-9567</issn><issn>1098-5522</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc1LAzEQxYMotlZvnmWPHtyaZDeb5CKUorVQv0DPIZudbSPbTU1Sof-9q61FT8MwP9483kPonOAhIVRcT0fTIcY5linhB6hPsBQpY5Qeoj7GRKaSFbyHTkJ479Y8z8Ux6lHBMyky0kcvj7CO3q0WtgnJyEMyhjZ63STRJaM22tJVm_QBKqsjVMmzdxFMtK5N9FzbNsRkAq2NHT9eNHq56bhTdFTrJsDZbg7Q293t6_g-nT1NpuPRLDWZwDFlooTOTAWUV1lOTa5rqA0GwsEwgkuZg4ayYIJpXhlTUlZJQYui5gWVBNNsgG62uqt1uYTKbH2rlbdL7TfKaav-X1q7UHP3qViBeU5EJ3C5E_DuYw0hqqUNBppGt-DWQRFJM0IKJmWHXm1R410IHur9G4LVdwuqa0H9tKAI7_CLv9b28G_s2RegHIQS</recordid><startdate>20171001</startdate><enddate>20171001</enddate><creator>Naglak, Elizabeth K</creator><creator>Morrison, Sandra G</creator><creator>Morrison, Richard P</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/0000-0002-9747-9884</orcidid></search><sort><creationdate>20171001</creationdate><title>Neutrophils Are Central to Antibody-Mediated Protection against Genital Chlamydia</title><author>Naglak, Elizabeth K ; Morrison, Sandra G ; Morrison, Richard P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c380t-58be448de27d342c4afefc0e17ec510b94eaeb6585a7dccb25d98266f76291023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Antibodies, Bacterial - blood</topic><topic>Antibodies, Bacterial - immunology</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>Chlamydia Infections - immunology</topic><topic>Chlamydia Infections - prevention & control</topic><topic>Chlamydia muridarum - immunology</topic><topic>Female</topic><topic>Genital Diseases, Female - immunology</topic><topic>Genital Diseases, Female - prevention & control</topic><topic>Genitalia - immunology</topic><topic>Genitalia - microbiology</topic><topic>Immunity, Humoral</topic><topic>Immunoglobulin G - blood</topic><topic>Immunoglobulin G - immunology</topic><topic>Interferon-gamma - immunology</topic><topic>Interferon-gamma - pharmacology</topic><topic>Killer Cells, Natural - immunology</topic><topic>Mice</topic><topic>Microbial Immunity and Vaccines</topic><topic>Neutrophils - drug effects</topic><topic>Neutrophils - immunology</topic><topic>Sexually Transmitted Diseases - immunology</topic><topic>Sexually Transmitted Diseases - microbiology</topic><topic>Sexually Transmitted Diseases - prevention & control</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Naglak, Elizabeth K</creatorcontrib><creatorcontrib>Morrison, Sandra G</creatorcontrib><creatorcontrib>Morrison, Richard P</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>Naglak, Elizabeth K</au><au>Morrison, Sandra G</au><au>Morrison, Richard P</au><au>Palmer, Guy H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neutrophils Are Central to Antibody-Mediated Protection against Genital Chlamydia</atitle><jtitle>Infection and immunity</jtitle><addtitle>Infect Immun</addtitle><date>2017-10-01</date><risdate>2017</risdate><volume>85</volume><issue>10</issue><issn>0019-9567</issn><eissn>1098-5522</eissn><abstract>Determining the effector populations involved in humoral protection against genital chlamydia infection is crucial to development of an effective chlamydial vaccine. Antibody has been implicated in protection studies in multiple animal models, and we previously showed that the passive transfer of immune serum alone does not confer immunity in the mouse. Using the
model of genital infection, we demonstrate a protective role for both
-specific immunoglobulin G (IgG) and polymorphonuclear neutrophils and show the importance of an antibody/effector cell interaction in mediating humoral immunity. While neutrophils were found to contribute significantly to antibody-mediated protection
, natural killer (NK) cells were dispensable for protective immunity. Furthermore, gamma interferon (IFN-γ)-stimulated primary peritoneal neutrophils (PPNs) killed chlamydiae
in an antibody-dependent manner. The results from this study support the view that an IFN-γ-activated effector cell population cooperates with antibody to protect against genital chlamydia and establish neutrophils as a key effector cell in this response.</abstract><cop>United States</cop><pub>American Society for Microbiology</pub><pmid>28739831</pmid><doi>10.1128/IAI.00409-17</doi><orcidid>https://orcid.org/0000-0002-9747-9884</orcidid><oa>free_for_read</oa></addata></record> |
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source | American Society for Microbiology; MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
subjects | Animals Antibodies, Bacterial - blood Antibodies, Bacterial - immunology CD4-Positive T-Lymphocytes - immunology Chlamydia Infections - immunology Chlamydia Infections - prevention & control Chlamydia muridarum - immunology Female Genital Diseases, Female - immunology Genital Diseases, Female - prevention & control Genitalia - immunology Genitalia - microbiology Immunity, Humoral Immunoglobulin G - blood Immunoglobulin G - immunology Interferon-gamma - immunology Interferon-gamma - pharmacology Killer Cells, Natural - immunology Mice Microbial Immunity and Vaccines Neutrophils - drug effects Neutrophils - immunology Sexually Transmitted Diseases - immunology Sexually Transmitted Diseases - microbiology Sexually Transmitted Diseases - prevention & control |
title | Neutrophils Are Central to Antibody-Mediated Protection against Genital Chlamydia |
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