Dysregulation in retinal para-inflammation and age-related retinal degeneration in CCL2 or CCR2 deficient mice
We have shown previously that a para-inflammatory response exists at the retinal/choroidal interface in the aging eye; and this response plays an important role in maintaining retinal homeostasis under chronic stress conditions. We hypothesized that dysregulation of the para-inflammatory response ma...
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| description | We have shown previously that a para-inflammatory response exists at the retinal/choroidal interface in the aging eye; and this response plays an important role in maintaining retinal homeostasis under chronic stress conditions. We hypothesized that dysregulation of the para-inflammatory response may result in an overt pro-inflammatory response inducing retinal degeneration. In this study, we examined this hypothesis in mice deficient in chemokine CCL2 or its cognate receptor CCR2. CCL2- or CCR2-deficient mice developed retinal degenerative changes with age, characterized as retinal pigment epithelial (RPE) cell and photoreceptor cell death. Retinal cell death was associated with significantly more subretinal microglial accumulation and increased complement activation. In addition, monocytes from CCL2- or CCR2-deficient mice had reduced capacity for phagocytosis and chemotaxis, expressed less IL-10 but more iNOS, IL-12 and TNF-α when compared to monocytes from WT mice. Complement activation at the site of RPE cell death resulted in C3b/C3d but not C5b-9 deposition, indicating only partial activation of the complement pathway. Our results suggest that altered monocyte functions may convert the protective para-inflammatory response into an overtly harmful inflammation at the retina/choroidal interface in CCL2- or CCR2-deficient mice, leading to RPE and photoreceptor degeneration. These data support a concept whereby a protective para-inflammatory response relies upon a normally functioning innate immune system. If the innate immune system is deficient chronic stress may tip the balance towards an overt inflammatory response causing cell/tissue damage. |
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We hypothesized that dysregulation of the para-inflammatory response may result in an overt pro-inflammatory response inducing retinal degeneration. In this study, we examined this hypothesis in mice deficient in chemokine CCL2 or its cognate receptor CCR2. CCL2- or CCR2-deficient mice developed retinal degenerative changes with age, characterized as retinal pigment epithelial (RPE) cell and photoreceptor cell death. Retinal cell death was associated with significantly more subretinal microglial accumulation and increased complement activation. In addition, monocytes from CCL2- or CCR2-deficient mice had reduced capacity for phagocytosis and chemotaxis, expressed less IL-10 but more iNOS, IL-12 and TNF-α when compared to monocytes from WT mice. Complement activation at the site of RPE cell death resulted in C3b/C3d but not C5b-9 deposition, indicating only partial activation of the complement pathway. Our results suggest that altered monocyte functions may convert the protective para-inflammatory response into an overtly harmful inflammation at the retina/choroidal interface in CCL2- or CCR2-deficient mice, leading to RPE and photoreceptor degeneration. These data support a concept whereby a protective para-inflammatory response relies upon a normally functioning innate immune system. If the innate immune system is deficient chronic stress may tip the balance towards an overt inflammatory response causing cell/tissue damage.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0022818</identifier><identifier>PMID: 21850237</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Age ; Aging ; Animals ; Autoimmune Diseases - genetics ; Autoimmune Diseases - metabolism ; Breakdowns ; CC chemokine receptors ; CCR2 protein ; Cell activation ; Cell death ; Chemokine CCL2 - deficiency ; Chemokine CCL2 - genetics ; Chemokines ; Chemotaxis ; Complement ; Complement activation ; Complement component C3b ; Cytokines ; Dendritic Cells - metabolism ; Female ; Free radicals ; Genes ; Homeostasis ; Hypotheses ; Immune system ; Inflammation ; Inflammatory response ; Innate immunity ; Interleukin 10 ; Interleukin 12 ; Interleukin-10 - metabolism ; Lasers ; Leukocytes, Mononuclear - metabolism ; Light ; Lymphatic system ; Macular degeneration ; Medicine ; Mice ; Mice, Knockout ; Microscopy, Electron, Transmission ; Monocyte chemoattractant protein 1 ; Monocytes ; Mortality ; Nitric Oxide Synthase Type II - metabolism ; Nitric-oxide synthase ; Phagocytosis ; Photoreceptors ; Physiological aspects ; Physiology ; Receptors, CCR2 - deficiency ; Receptors, CCR2 - genetics ; Retina ; Retina - metabolism ; Retina - pathology ; Retina - ultrastructure ; Retinal degeneration ; Retinal Diseases - genetics ; Retinal Diseases - metabolism ; Retinal Diseases - pathology ; Retinal Pigment Epithelium - metabolism ; Retinal Pigment Epithelium - pathology ; Rodents ; Stress (Psychology) ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-α</subject><ispartof>PloS one, 2011-08, Vol.6 (8), p.e22818-e22818</ispartof><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Chen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://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>Chen et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c691t-a5580868f6dc116e1f4fa83d69c097c99831117cc67977de582526d6348533173</citedby><cites>FETCH-LOGICAL-c691t-a5580868f6dc116e1f4fa83d69c097c99831117cc67977de582526d6348533173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3151263/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3151263/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21850237$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Klein, Robyn</contributor><creatorcontrib>Chen, Mei</creatorcontrib><creatorcontrib>Forrester, John V</creatorcontrib><creatorcontrib>Xu, Heping</creatorcontrib><title>Dysregulation in retinal para-inflammation and age-related retinal degeneration in CCL2 or CCR2 deficient mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>We have shown previously that a para-inflammatory response exists at the retinal/choroidal interface in the aging eye; and this response plays an important role in maintaining retinal homeostasis under chronic stress conditions. We hypothesized that dysregulation of the para-inflammatory response may result in an overt pro-inflammatory response inducing retinal degeneration. In this study, we examined this hypothesis in mice deficient in chemokine CCL2 or its cognate receptor CCR2. CCL2- or CCR2-deficient mice developed retinal degenerative changes with age, characterized as retinal pigment epithelial (RPE) cell and photoreceptor cell death. Retinal cell death was associated with significantly more subretinal microglial accumulation and increased complement activation. In addition, monocytes from CCL2- or CCR2-deficient mice had reduced capacity for phagocytosis and chemotaxis, expressed less IL-10 but more iNOS, IL-12 and TNF-α when compared to monocytes from WT mice. Complement activation at the site of RPE cell death resulted in C3b/C3d but not C5b-9 deposition, indicating only partial activation of the complement pathway. Our results suggest that altered monocyte functions may convert the protective para-inflammatory response into an overtly harmful inflammation at the retina/choroidal interface in CCL2- or CCR2-deficient mice, leading to RPE and photoreceptor degeneration. These data support a concept whereby a protective para-inflammatory response relies upon a normally functioning innate immune system. If the innate immune system is deficient chronic stress may tip the balance towards an overt inflammatory response causing cell/tissue damage.</description><subject>Age</subject><subject>Aging</subject><subject>Animals</subject><subject>Autoimmune Diseases - genetics</subject><subject>Autoimmune Diseases - metabolism</subject><subject>Breakdowns</subject><subject>CC chemokine receptors</subject><subject>CCR2 protein</subject><subject>Cell activation</subject><subject>Cell death</subject><subject>Chemokine CCL2 - deficiency</subject><subject>Chemokine CCL2 - genetics</subject><subject>Chemokines</subject><subject>Chemotaxis</subject><subject>Complement</subject><subject>Complement activation</subject><subject>Complement component C3b</subject><subject>Cytokines</subject><subject>Dendritic Cells - metabolism</subject><subject>Female</subject><subject>Free radicals</subject><subject>Genes</subject><subject>Homeostasis</subject><subject>Hypotheses</subject><subject>Immune system</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Innate immunity</subject><subject>Interleukin 10</subject><subject>Interleukin 12</subject><subject>Interleukin-10 - metabolism</subject><subject>Lasers</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Light</subject><subject>Lymphatic system</subject><subject>Macular degeneration</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Microscopy, Electron, Transmission</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>Mortality</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Nitric-oxide synthase</subject><subject>Phagocytosis</subject><subject>Photoreceptors</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Receptors, CCR2 - deficiency</subject><subject>Receptors, CCR2 - genetics</subject><subject>Retina</subject><subject>Retina - metabolism</subject><subject>Retina - pathology</subject><subject>Retina - ultrastructure</subject><subject>Retinal degeneration</subject><subject>Retinal Diseases - genetics</subject><subject>Retinal Diseases - metabolism</subject><subject>Retinal Diseases - pathology</subject><subject>Retinal Pigment Epithelium - metabolism</subject><subject>Retinal Pigment Epithelium - pathology</subject><subject>Rodents</subject><subject>Stress (Psychology)</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-α</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk1uL1DAUx4so7rr6DUQLguJDx1zaNH0RlvE2MLCwXl5DJjntZEmTMWnF_fZmnO4wlX2QPqTk_M7_5Nyy7DlGC0xr_O7Gj8FJu9h5BwuECOGYP8jOcUNJwQiiD0_-z7InMd4gVFHO2OPsjGBeIULr88x9uI0ButHKwXiXG5cHGEzSzXcyyMK41sq-Pxil07nsoAiQaNBHUkMHDsJRYblck9yHdF6TZGyNMuCGvDcKnmaPWmkjPJvOi-z7p4_fll-K9dXn1fJyXSjW4KGQVcURZ7xlWmHMALdlKznVrFGoqVXTcIoxrpVidVPXGipOKsI0oyWvKMU1vcheHnR31kcxlSoKTBHjTc1LlIjVgdBe3ohdML0Mt8JLI_5e-NAJGQajLIiNBqSBAQXKS7nRTQoOdVuWrEKAOE5a76do46YHrVK2QdqZ6NzizFZ0_peguMKE0STwZhII_ucIcRC9iQqslQ78GAXnZUnKlGQiX_1D3p_cRHUyvT810aewaq8pLsuacU4avi_S4h4qfRpSr9JYtSbdzxzezhwSM8DvoZNjjGL19fr_2asfc_b1CbsFaYdt9HbcD1Scg-UBVMHHNLftscYYif1W3FVD7LdCTFuR3F6c9ufodLcG9A-CZwYW</recordid><startdate>20110805</startdate><enddate>20110805</enddate><creator>Chen, Mei</creator><creator>Forrester, John V</creator><creator>Xu, Heping</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20110805</creationdate><title>Dysregulation in retinal para-inflammation and age-related retinal degeneration in CCL2 or CCR2 deficient mice</title><author>Chen, Mei ; Forrester, John V ; Xu, Heping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c691t-a5580868f6dc116e1f4fa83d69c097c99831117cc67977de582526d6348533173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Age</topic><topic>Aging</topic><topic>Animals</topic><topic>Autoimmune Diseases - genetics</topic><topic>Autoimmune Diseases - metabolism</topic><topic>Breakdowns</topic><topic>CC chemokine receptors</topic><topic>CCR2 protein</topic><topic>Cell activation</topic><topic>Cell death</topic><topic>Chemokine CCL2 - deficiency</topic><topic>Chemokine CCL2 - genetics</topic><topic>Chemokines</topic><topic>Chemotaxis</topic><topic>Complement</topic><topic>Complement activation</topic><topic>Complement component C3b</topic><topic>Cytokines</topic><topic>Dendritic Cells - metabolism</topic><topic>Female</topic><topic>Free radicals</topic><topic>Genes</topic><topic>Homeostasis</topic><topic>Hypotheses</topic><topic>Immune system</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Innate immunity</topic><topic>Interleukin 10</topic><topic>Interleukin 12</topic><topic>Interleukin-10 - metabolism</topic><topic>Lasers</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Light</topic><topic>Lymphatic system</topic><topic>Macular degeneration</topic><topic>Medicine</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Microscopy, Electron, Transmission</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Monocytes</topic><topic>Mortality</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Nitric-oxide synthase</topic><topic>Phagocytosis</topic><topic>Photoreceptors</topic><topic>Physiological aspects</topic><topic>Physiology</topic><topic>Receptors, CCR2 - deficiency</topic><topic>Receptors, CCR2 - genetics</topic><topic>Retina</topic><topic>Retina - metabolism</topic><topic>Retina - pathology</topic><topic>Retina - ultrastructure</topic><topic>Retinal degeneration</topic><topic>Retinal Diseases - genetics</topic><topic>Retinal Diseases - metabolism</topic><topic>Retinal Diseases - pathology</topic><topic>Retinal Pigment Epithelium - metabolism</topic><topic>Retinal Pigment Epithelium - pathology</topic><topic>Rodents</topic><topic>Stress (Psychology)</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Mei</creatorcontrib><creatorcontrib>Forrester, John V</creatorcontrib><creatorcontrib>Xu, Heping</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Mei</au><au>Forrester, John V</au><au>Xu, Heping</au><au>Klein, Robyn</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dysregulation in retinal para-inflammation and age-related retinal degeneration in CCL2 or CCR2 deficient mice</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2011-08-05</date><risdate>2011</risdate><volume>6</volume><issue>8</issue><spage>e22818</spage><epage>e22818</epage><pages>e22818-e22818</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>We have shown previously that a para-inflammatory response exists at the retinal/choroidal interface in the aging eye; and this response plays an important role in maintaining retinal homeostasis under chronic stress conditions. We hypothesized that dysregulation of the para-inflammatory response may result in an overt pro-inflammatory response inducing retinal degeneration. In this study, we examined this hypothesis in mice deficient in chemokine CCL2 or its cognate receptor CCR2. CCL2- or CCR2-deficient mice developed retinal degenerative changes with age, characterized as retinal pigment epithelial (RPE) cell and photoreceptor cell death. Retinal cell death was associated with significantly more subretinal microglial accumulation and increased complement activation. In addition, monocytes from CCL2- or CCR2-deficient mice had reduced capacity for phagocytosis and chemotaxis, expressed less IL-10 but more iNOS, IL-12 and TNF-α when compared to monocytes from WT mice. Complement activation at the site of RPE cell death resulted in C3b/C3d but not C5b-9 deposition, indicating only partial activation of the complement pathway. Our results suggest that altered monocyte functions may convert the protective para-inflammatory response into an overtly harmful inflammation at the retina/choroidal interface in CCL2- or CCR2-deficient mice, leading to RPE and photoreceptor degeneration. These data support a concept whereby a protective para-inflammatory response relies upon a normally functioning innate immune system. If the innate immune system is deficient chronic stress may tip the balance towards an overt inflammatory response causing cell/tissue damage.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>21850237</pmid><doi>10.1371/journal.pone.0022818</doi><tpages>e22818</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1932-6203 1932-6203 |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Age Aging Animals Autoimmune Diseases - genetics Autoimmune Diseases - metabolism Breakdowns CC chemokine receptors CCR2 protein Cell activation Cell death Chemokine CCL2 - deficiency Chemokine CCL2 - genetics Chemokines Chemotaxis Complement Complement activation Complement component C3b Cytokines Dendritic Cells - metabolism Female Free radicals Genes Homeostasis Hypotheses Immune system Inflammation Inflammatory response Innate immunity Interleukin 10 Interleukin 12 Interleukin-10 - metabolism Lasers Leukocytes, Mononuclear - metabolism Light Lymphatic system Macular degeneration Medicine Mice Mice, Knockout Microscopy, Electron, Transmission Monocyte chemoattractant protein 1 Monocytes Mortality Nitric Oxide Synthase Type II - metabolism Nitric-oxide synthase Phagocytosis Photoreceptors Physiological aspects Physiology Receptors, CCR2 - deficiency Receptors, CCR2 - genetics Retina Retina - metabolism Retina - pathology Retina - ultrastructure Retinal degeneration Retinal Diseases - genetics Retinal Diseases - metabolism Retinal Diseases - pathology Retinal Pigment Epithelium - metabolism Retinal Pigment Epithelium - pathology Rodents Stress (Psychology) Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-α |
| title | Dysregulation in retinal para-inflammation and age-related retinal degeneration in CCL2 or CCR2 deficient mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T03%3A29%3A59IST&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=Dysregulation%20in%20retinal%20para-inflammation%20and%20age-related%20retinal%20degeneration%20in%20CCL2%20or%20CCR2%20deficient%20mice&rft.jtitle=PloS%20one&rft.au=Chen,%20Mei&rft.date=2011-08-05&rft.volume=6&rft.issue=8&rft.spage=e22818&rft.epage=e22818&rft.pages=e22818-e22818&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0022818&rft_dat=%3Cgale_plos_%3EA476882987%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=1306897840&rft_id=info:pmid/21850237&rft_galeid=A476882987&rft_doaj_id=oai_doaj_org_article_bde0de6e3e384abd9311e7f44650e081&rfr_iscdi=true |