Adipose Recruitment and Activation of Plasmacytoid Dendritic Cells Fuel Metaflammation
In obese individuals, visceral adipose tissue (VAT) is the seat of chronic low-grade inflammation (metaflammation), but the mechanistic link between increased adiposity and metaflammation largely remains unclear. In obese individuals, deregulation of a specific adipokine, chemerin, contributes to in...
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| Veröffentlicht in: | Diabetes (New York, N.Y.) N.Y.), 2016-11, Vol.65 (11), p.3440-3452 |
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| creator | Ghosh, Amrit Raj Bhattacharya, Roopkatha Bhattacharya, Shamik Nargis, Titli Rahaman, Oindrila Duttagupta, Pritam Raychaudhuri, Deblina Liu, Chinky Shiu Chen Roy, Shounak Ghosh, Parasar Khanna, Shashi Chaudhuri, Tamonas Tantia, Om Haak, Stefan Bandyopadhyay, Santu Mukhopadhyay, Satinath Chakrabarti, Partha Ganguly, Dipyaman |
| description | In obese individuals, visceral adipose tissue (VAT) is the seat of chronic low-grade inflammation (metaflammation), but the mechanistic link between increased adiposity and metaflammation largely remains unclear. In obese individuals, deregulation of a specific adipokine, chemerin, contributes to innate initiation of metaflammation by recruiting circulating plasmacytoid dendritic cells (pDCs) into VAT through chemokine-like receptor 1 (CMKLR1). Adipose tissue-derived high-mobility group B1 (HMGB1) protein activates Toll-like receptor 9 (TLR9) in the adipose-recruited pDCs by transporting extracellular DNA through receptor for advanced glycation end products (RAGE) and induces production of type I interferons (IFNs). Type I IFNs in turn help in proinflammatory polarization of adipose-resident macrophages. IFN signature gene expression in VAT correlates with both adipose tissue and systemic insulin resistance (IR) in obese individuals, which is represented by ADIPO-IR and HOMA2-IR, respectively, and defines two subgroups with different susceptibility to IR. Thus, this study reveals a pathway that drives adipose tissue inflammation and consequent IR in obesity. |
| doi_str_mv | 10.2337/db16-0331 |
| format | Article |
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In obese individuals, deregulation of a specific adipokine, chemerin, contributes to innate initiation of metaflammation by recruiting circulating plasmacytoid dendritic cells (pDCs) into VAT through chemokine-like receptor 1 (CMKLR1). Adipose tissue-derived high-mobility group B1 (HMGB1) protein activates Toll-like receptor 9 (TLR9) in the adipose-recruited pDCs by transporting extracellular DNA through receptor for advanced glycation end products (RAGE) and induces production of type I interferons (IFNs). Type I IFNs in turn help in proinflammatory polarization of adipose-resident macrophages. IFN signature gene expression in VAT correlates with both adipose tissue and systemic insulin resistance (IR) in obese individuals, which is represented by ADIPO-IR and HOMA2-IR, respectively, and defines two subgroups with different susceptibility to IR. Thus, this study reveals a pathway that drives adipose tissue inflammation and consequent IR in obesity.</description><identifier>ISSN: 0012-1797</identifier><identifier>EISSN: 1939-327X</identifier><identifier>DOI: 10.2337/db16-0331</identifier><identifier>PMID: 27561727</identifier><identifier>CODEN: DIAEAZ</identifier><language>eng</language><publisher>United States: American Diabetes Association</publisher><subject>Adipocytes ; Adipose Tissue - metabolism ; Adult ; Aged ; Aged, 80 and over ; Chemokines ; Dendritic cells ; Dendritic Cells - metabolism ; Diabetes ; Female ; Glycation End Products, Advanced - metabolism ; HMGB1 Protein - genetics ; HMGB1 Protein - metabolism ; Humans ; Inflammation ; Inflammation - metabolism ; Insulin resistance ; Insulin Resistance - genetics ; Insulin Resistance - physiology ; Interferon Type I - genetics ; Interferon Type I - metabolism ; Intra-Abdominal Fat - metabolism ; Male ; Middle Aged ; Obesity ; Receptors, G-Protein-Coupled - genetics ; Receptors, G-Protein-Coupled - metabolism ; Toll-Like Receptor 9 - genetics ; Toll-Like Receptor 9 - metabolism</subject><ispartof>Diabetes (New York, N.Y.), 2016-11, Vol.65 (11), p.3440-3452</ispartof><rights>2016 by the American Diabetes Association.</rights><rights>Copyright American Diabetes Association Nov 1, 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c414t-f74632c95fcdd2fe74e22c19a1896610499b61bafae914ba3e111632a6d1e4803</citedby><cites>FETCH-LOGICAL-c414t-f74632c95fcdd2fe74e22c19a1896610499b61bafae914ba3e111632a6d1e4803</cites><orcidid>0000-0002-7786-1795</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27561727$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ghosh, Amrit Raj</creatorcontrib><creatorcontrib>Bhattacharya, Roopkatha</creatorcontrib><creatorcontrib>Bhattacharya, Shamik</creatorcontrib><creatorcontrib>Nargis, Titli</creatorcontrib><creatorcontrib>Rahaman, Oindrila</creatorcontrib><creatorcontrib>Duttagupta, Pritam</creatorcontrib><creatorcontrib>Raychaudhuri, Deblina</creatorcontrib><creatorcontrib>Liu, Chinky Shiu Chen</creatorcontrib><creatorcontrib>Roy, Shounak</creatorcontrib><creatorcontrib>Ghosh, Parasar</creatorcontrib><creatorcontrib>Khanna, Shashi</creatorcontrib><creatorcontrib>Chaudhuri, Tamonas</creatorcontrib><creatorcontrib>Tantia, Om</creatorcontrib><creatorcontrib>Haak, Stefan</creatorcontrib><creatorcontrib>Bandyopadhyay, Santu</creatorcontrib><creatorcontrib>Mukhopadhyay, Satinath</creatorcontrib><creatorcontrib>Chakrabarti, Partha</creatorcontrib><creatorcontrib>Ganguly, Dipyaman</creatorcontrib><title>Adipose Recruitment and Activation of Plasmacytoid Dendritic Cells Fuel Metaflammation</title><title>Diabetes (New York, N.Y.)</title><addtitle>Diabetes</addtitle><description>In obese individuals, visceral adipose tissue (VAT) is the seat of chronic low-grade inflammation (metaflammation), but the mechanistic link between increased adiposity and metaflammation largely remains unclear. In obese individuals, deregulation of a specific adipokine, chemerin, contributes to innate initiation of metaflammation by recruiting circulating plasmacytoid dendritic cells (pDCs) into VAT through chemokine-like receptor 1 (CMKLR1). Adipose tissue-derived high-mobility group B1 (HMGB1) protein activates Toll-like receptor 9 (TLR9) in the adipose-recruited pDCs by transporting extracellular DNA through receptor for advanced glycation end products (RAGE) and induces production of type I interferons (IFNs). Type I IFNs in turn help in proinflammatory polarization of adipose-resident macrophages. IFN signature gene expression in VAT correlates with both adipose tissue and systemic insulin resistance (IR) in obese individuals, which is represented by ADIPO-IR and HOMA2-IR, respectively, and defines two subgroups with different susceptibility to IR. Thus, this study reveals a pathway that drives adipose tissue inflammation and consequent IR in obesity.</description><subject>Adipocytes</subject><subject>Adipose Tissue - metabolism</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Chemokines</subject><subject>Dendritic cells</subject><subject>Dendritic Cells - metabolism</subject><subject>Diabetes</subject><subject>Female</subject><subject>Glycation End Products, Advanced - metabolism</subject><subject>HMGB1 Protein - genetics</subject><subject>HMGB1 Protein - metabolism</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - genetics</subject><subject>Insulin Resistance - physiology</subject><subject>Interferon Type I - genetics</subject><subject>Interferon Type I - metabolism</subject><subject>Intra-Abdominal Fat - metabolism</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Obesity</subject><subject>Receptors, G-Protein-Coupled - genetics</subject><subject>Receptors, G-Protein-Coupled - metabolism</subject><subject>Toll-Like Receptor 9 - genetics</subject><subject>Toll-Like Receptor 9 - metabolism</subject><issn>0012-1797</issn><issn>1939-327X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkEFLHTEUhYO06OvThX9AAt3UxbS5SSaZLB-v2hYsFVFxN2SSG4jMTF4nmYL_3nlquyh3cTbfOVw-Qk6BfeZC6C--A1UxIeCArMAIUwmuH96RFWPAK9BGH5EPOT8yxtRyh-SI61qB5npF7jc-7lJGeoNummMZcCzUjp5uXIl_bIlppCnQ697mwbqnkqKnX3H0UyzR0S32faaXM_b0JxYbejsML51j8j7YPuPJW67J3eXF7fZ7dfXr24_t5qpyEmSpgpZKcGfq4LznAbVEzh0YC41RCpg0plPQ2WDRgOysQABYGlZ5QNkwsSafXnd3U_o9Yy7tELNbvrIjpjm30NRc1bJpzIJ-_A99TPM0Lt8tlDCyrs2Sa3L-Srkp5TxhaHdTHOz01AJr97Lbvex2L3thz94W525A_4_8a1c8A_3TeOI</recordid><startdate>20161101</startdate><enddate>20161101</enddate><creator>Ghosh, Amrit Raj</creator><creator>Bhattacharya, Roopkatha</creator><creator>Bhattacharya, Shamik</creator><creator>Nargis, Titli</creator><creator>Rahaman, Oindrila</creator><creator>Duttagupta, Pritam</creator><creator>Raychaudhuri, Deblina</creator><creator>Liu, Chinky Shiu Chen</creator><creator>Roy, Shounak</creator><creator>Ghosh, Parasar</creator><creator>Khanna, Shashi</creator><creator>Chaudhuri, Tamonas</creator><creator>Tantia, Om</creator><creator>Haak, Stefan</creator><creator>Bandyopadhyay, Santu</creator><creator>Mukhopadhyay, Satinath</creator><creator>Chakrabarti, Partha</creator><creator>Ganguly, Dipyaman</creator><general>American Diabetes Association</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>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7786-1795</orcidid></search><sort><creationdate>20161101</creationdate><title>Adipose Recruitment and Activation of Plasmacytoid Dendritic Cells Fuel Metaflammation</title><author>Ghosh, Amrit Raj ; 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In obese individuals, deregulation of a specific adipokine, chemerin, contributes to innate initiation of metaflammation by recruiting circulating plasmacytoid dendritic cells (pDCs) into VAT through chemokine-like receptor 1 (CMKLR1). Adipose tissue-derived high-mobility group B1 (HMGB1) protein activates Toll-like receptor 9 (TLR9) in the adipose-recruited pDCs by transporting extracellular DNA through receptor for advanced glycation end products (RAGE) and induces production of type I interferons (IFNs). Type I IFNs in turn help in proinflammatory polarization of adipose-resident macrophages. IFN signature gene expression in VAT correlates with both adipose tissue and systemic insulin resistance (IR) in obese individuals, which is represented by ADIPO-IR and HOMA2-IR, respectively, and defines two subgroups with different susceptibility to IR. Thus, this study reveals a pathway that drives adipose tissue inflammation and consequent IR in obesity.</abstract><cop>United States</cop><pub>American Diabetes Association</pub><pmid>27561727</pmid><doi>10.2337/db16-0331</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-7786-1795</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adipocytes Adipose Tissue - metabolism Adult Aged Aged, 80 and over Chemokines Dendritic cells Dendritic Cells - metabolism Diabetes Female Glycation End Products, Advanced - metabolism HMGB1 Protein - genetics HMGB1 Protein - metabolism Humans Inflammation Inflammation - metabolism Insulin resistance Insulin Resistance - genetics Insulin Resistance - physiology Interferon Type I - genetics Interferon Type I - metabolism Intra-Abdominal Fat - metabolism Male Middle Aged Obesity Receptors, G-Protein-Coupled - genetics Receptors, G-Protein-Coupled - metabolism Toll-Like Receptor 9 - genetics Toll-Like Receptor 9 - metabolism |
| title | Adipose Recruitment and Activation of Plasmacytoid Dendritic Cells Fuel Metaflammation |
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