Epigenetic Regulation of TLR4 in Diabetic Macrophages Modulates Immunometabolism and Wound Repair
Macrophages are critical for the initiation and resolution of the inflammatory phase of wound healing. In diabetes, macrophages display a prolonged inflammatory phenotype preventing tissue repair. TLRs, particularly TLR4, have been shown to regulate myeloid-mediated inflammation in wounds. We examin...
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| Veröffentlicht in: | The Journal of immunology (1950) 2020-05, Vol.204 (9), p.2503-2513 |
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| creator | Davis, Frank M denDekker, Aaron Kimball, Andrew Joshi, Amrita D El Azzouny, Mahmoud Wolf, Sonya J Obi, Andrea T Lipinski, Jay Gudjonsson, Johann E Xing, Xianying Plazyo, Olesya Audu, Christopher Melvin, William J Singer, Kanakadurga Henke, Peter K Moore, Bethany B Burant, Charles Kunkel, Steven L Gallagher, Katherine A |
| description | Macrophages are critical for the initiation and resolution of the inflammatory phase of wound healing. In diabetes, macrophages display a prolonged inflammatory phenotype preventing tissue repair. TLRs, particularly TLR4, have been shown to regulate myeloid-mediated inflammation in wounds. We examined macrophages isolated from wounds of patients afflicted with diabetes and healthy controls as well as a murine diabetic model demonstrating dynamic expression of TLR4 results in altered metabolic pathways in diabetic macrophages. Further, using a myeloid-specific mixed-lineage leukemia 1 (MLL1) knockout (
), we determined that MLL1 drives
expression in diabetic macrophages by regulating levels of histone H3 lysine 4 trimethylation on the
promoter. Mechanistically, MLL1-mediated epigenetic alterations influence diabetic macrophage responsiveness to TLR4 stimulation and inhibit tissue repair. Pharmacological inhibition of the TLR4 pathway using a small molecule inhibitor (TAK-242) as well as genetic depletion of either
(
) or myeloid-specific
resulted in improved diabetic wound healing. These results define an important role for MLL1-mediated epigenetic regulation of TLR4 in pathologic diabetic wound repair and suggest a target for therapeutic manipulation. |
| doi_str_mv | 10.4049/jimmunol.1901263 |
| format | Article |
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), we determined that MLL1 drives
expression in diabetic macrophages by regulating levels of histone H3 lysine 4 trimethylation on the
promoter. Mechanistically, MLL1-mediated epigenetic alterations influence diabetic macrophage responsiveness to TLR4 stimulation and inhibit tissue repair. Pharmacological inhibition of the TLR4 pathway using a small molecule inhibitor (TAK-242) as well as genetic depletion of either
(
) or myeloid-specific
resulted in improved diabetic wound healing. These results define an important role for MLL1-mediated epigenetic regulation of TLR4 in pathologic diabetic wound repair and suggest a target for therapeutic manipulation.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.1901263</identifier><identifier>PMID: 32205424</identifier><language>eng</language><publisher>United States</publisher><subject>Aged ; Animals ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - immunology ; Epigenesis, Genetic - genetics ; Epigenesis, Genetic - immunology ; Female ; Histones - genetics ; Histones - immunology ; Humans ; Inflammation - genetics ; Inflammation - immunology ; Inflammation Mediators - immunology ; Macrophages - immunology ; Macrophages - physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Middle Aged ; Myeloid-Lymphoid Leukemia Protein - genetics ; Myeloid-Lymphoid Leukemia Protein - immunology ; Promoter Regions, Genetic - genetics ; Promoter Regions, Genetic - immunology ; Toll-Like Receptor 4 - genetics ; Toll-Like Receptor 4 - immunology ; Wound Healing - genetics ; Wound Healing - immunology</subject><ispartof>The Journal of immunology (1950), 2020-05, Vol.204 (9), p.2503-2513</ispartof><rights>Copyright © 2020 by The American Association of Immunologists, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-a12500209dca82aa7a2e9eb5eaa5598610c8635d376c83ac54c2e2d941327eb03</citedby><cites>FETCH-LOGICAL-c396t-a12500209dca82aa7a2e9eb5eaa5598610c8635d376c83ac54c2e2d941327eb03</cites><orcidid>0000-0001-9189-5003 ; 0000-0001-7613-2366 ; 0000-0002-3241-5919 ; 0000-0002-6859-7590 ; 0000-0002-5847-8993 ; 0000-0001-8278-3800 ; 0000-0001-9604-0557 ; 0000-0002-0080-0812 ; 0000-0003-3051-745X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32205424$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Davis, Frank M</creatorcontrib><creatorcontrib>denDekker, Aaron</creatorcontrib><creatorcontrib>Kimball, Andrew</creatorcontrib><creatorcontrib>Joshi, Amrita D</creatorcontrib><creatorcontrib>El Azzouny, Mahmoud</creatorcontrib><creatorcontrib>Wolf, Sonya J</creatorcontrib><creatorcontrib>Obi, Andrea T</creatorcontrib><creatorcontrib>Lipinski, Jay</creatorcontrib><creatorcontrib>Gudjonsson, Johann E</creatorcontrib><creatorcontrib>Xing, Xianying</creatorcontrib><creatorcontrib>Plazyo, Olesya</creatorcontrib><creatorcontrib>Audu, Christopher</creatorcontrib><creatorcontrib>Melvin, William J</creatorcontrib><creatorcontrib>Singer, Kanakadurga</creatorcontrib><creatorcontrib>Henke, Peter K</creatorcontrib><creatorcontrib>Moore, Bethany B</creatorcontrib><creatorcontrib>Burant, Charles</creatorcontrib><creatorcontrib>Kunkel, Steven L</creatorcontrib><creatorcontrib>Gallagher, Katherine A</creatorcontrib><title>Epigenetic Regulation of TLR4 in Diabetic Macrophages Modulates Immunometabolism and Wound Repair</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Macrophages are critical for the initiation and resolution of the inflammatory phase of wound healing. In diabetes, macrophages display a prolonged inflammatory phenotype preventing tissue repair. TLRs, particularly TLR4, have been shown to regulate myeloid-mediated inflammation in wounds. We examined macrophages isolated from wounds of patients afflicted with diabetes and healthy controls as well as a murine diabetic model demonstrating dynamic expression of TLR4 results in altered metabolic pathways in diabetic macrophages. Further, using a myeloid-specific mixed-lineage leukemia 1 (MLL1) knockout (
), we determined that MLL1 drives
expression in diabetic macrophages by regulating levels of histone H3 lysine 4 trimethylation on the
promoter. Mechanistically, MLL1-mediated epigenetic alterations influence diabetic macrophage responsiveness to TLR4 stimulation and inhibit tissue repair. Pharmacological inhibition of the TLR4 pathway using a small molecule inhibitor (TAK-242) as well as genetic depletion of either
(
) or myeloid-specific
resulted in improved diabetic wound healing. These results define an important role for MLL1-mediated epigenetic regulation of TLR4 in pathologic diabetic wound repair and suggest a target for therapeutic manipulation.</description><subject>Aged</subject><subject>Animals</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - immunology</subject><subject>Epigenesis, Genetic - genetics</subject><subject>Epigenesis, Genetic - immunology</subject><subject>Female</subject><subject>Histones - genetics</subject><subject>Histones - immunology</subject><subject>Humans</subject><subject>Inflammation - genetics</subject><subject>Inflammation - immunology</subject><subject>Inflammation Mediators - immunology</subject><subject>Macrophages - immunology</subject><subject>Macrophages - physiology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Middle Aged</subject><subject>Myeloid-Lymphoid Leukemia Protein - genetics</subject><subject>Myeloid-Lymphoid Leukemia Protein - immunology</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Promoter Regions, Genetic - immunology</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-Like Receptor 4 - immunology</subject><subject>Wound Healing - genetics</subject><subject>Wound Healing - immunology</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUU1r20AQXUpK47i99xR0zEXu7KekS6AkTmJwKJiUHpfRamxvkLSqVgr031dO7NBeZgbemzePeYx95bBQoIpvz75pxjbUC14AF0Z-YDOuNaTGgDljMwAhUp6Z7JxdxPgMAAaE-sTOpRCglVAzhsvO76ilwbtkQ7uxxsGHNgnb5Gm9UYlvk1uP5Sv8iK4P3R53FJPHUB2o07R6ddDQgGWofWwSbKvkVxinuqEOff-ZfdxiHenLsc_Zz7vl081Duv5xv7r5vk6dLMyQIhd68gtF5TAXiBkKKqjUhKh1kRsOLjdSVzIzLpfotHKCRFUoLkVGJcg5u37T7cayocpRO_RY2673DfZ_bEBv_0dav7e78GIzpaQ0chK4Ogr04fdIcbCNj47qGlsKY7RC5sKYzGg9UeGNOn0kxp6272c42EMy9pSMPSYzrVz-a-994RSF_AuTQo1v</recordid><startdate>20200501</startdate><enddate>20200501</enddate><creator>Davis, Frank M</creator><creator>denDekker, Aaron</creator><creator>Kimball, Andrew</creator><creator>Joshi, Amrita D</creator><creator>El Azzouny, Mahmoud</creator><creator>Wolf, Sonya J</creator><creator>Obi, Andrea T</creator><creator>Lipinski, Jay</creator><creator>Gudjonsson, Johann E</creator><creator>Xing, Xianying</creator><creator>Plazyo, Olesya</creator><creator>Audu, Christopher</creator><creator>Melvin, William J</creator><creator>Singer, Kanakadurga</creator><creator>Henke, Peter K</creator><creator>Moore, Bethany B</creator><creator>Burant, Charles</creator><creator>Kunkel, Steven L</creator><creator>Gallagher, Katherine A</creator><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/0000-0001-9189-5003</orcidid><orcidid>https://orcid.org/0000-0001-7613-2366</orcidid><orcidid>https://orcid.org/0000-0002-3241-5919</orcidid><orcidid>https://orcid.org/0000-0002-6859-7590</orcidid><orcidid>https://orcid.org/0000-0002-5847-8993</orcidid><orcidid>https://orcid.org/0000-0001-8278-3800</orcidid><orcidid>https://orcid.org/0000-0001-9604-0557</orcidid><orcidid>https://orcid.org/0000-0002-0080-0812</orcidid><orcidid>https://orcid.org/0000-0003-3051-745X</orcidid></search><sort><creationdate>20200501</creationdate><title>Epigenetic Regulation of TLR4 in Diabetic Macrophages Modulates Immunometabolism and Wound Repair</title><author>Davis, Frank M ; denDekker, Aaron ; Kimball, Andrew ; Joshi, Amrita D ; El Azzouny, Mahmoud ; Wolf, Sonya J ; Obi, Andrea T ; Lipinski, Jay ; Gudjonsson, Johann E ; Xing, Xianying ; Plazyo, Olesya ; Audu, Christopher ; Melvin, William J ; Singer, Kanakadurga ; Henke, Peter K ; Moore, Bethany B ; Burant, Charles ; Kunkel, Steven L ; Gallagher, Katherine A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-a12500209dca82aa7a2e9eb5eaa5598610c8635d376c83ac54c2e2d941327eb03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aged</topic><topic>Animals</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - immunology</topic><topic>Epigenesis, Genetic - genetics</topic><topic>Epigenesis, Genetic - immunology</topic><topic>Female</topic><topic>Histones - genetics</topic><topic>Histones - immunology</topic><topic>Humans</topic><topic>Inflammation - genetics</topic><topic>Inflammation - immunology</topic><topic>Inflammation Mediators - immunology</topic><topic>Macrophages - immunology</topic><topic>Macrophages - physiology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Middle Aged</topic><topic>Myeloid-Lymphoid Leukemia Protein - genetics</topic><topic>Myeloid-Lymphoid Leukemia Protein - immunology</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Promoter Regions, Genetic - immunology</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-Like Receptor 4 - immunology</topic><topic>Wound Healing - genetics</topic><topic>Wound Healing - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Davis, Frank M</creatorcontrib><creatorcontrib>denDekker, Aaron</creatorcontrib><creatorcontrib>Kimball, Andrew</creatorcontrib><creatorcontrib>Joshi, Amrita D</creatorcontrib><creatorcontrib>El Azzouny, Mahmoud</creatorcontrib><creatorcontrib>Wolf, Sonya J</creatorcontrib><creatorcontrib>Obi, Andrea T</creatorcontrib><creatorcontrib>Lipinski, Jay</creatorcontrib><creatorcontrib>Gudjonsson, Johann E</creatorcontrib><creatorcontrib>Xing, Xianying</creatorcontrib><creatorcontrib>Plazyo, Olesya</creatorcontrib><creatorcontrib>Audu, Christopher</creatorcontrib><creatorcontrib>Melvin, William J</creatorcontrib><creatorcontrib>Singer, Kanakadurga</creatorcontrib><creatorcontrib>Henke, Peter K</creatorcontrib><creatorcontrib>Moore, Bethany B</creatorcontrib><creatorcontrib>Burant, Charles</creatorcontrib><creatorcontrib>Kunkel, Steven L</creatorcontrib><creatorcontrib>Gallagher, Katherine A</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>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Davis, Frank M</au><au>denDekker, Aaron</au><au>Kimball, Andrew</au><au>Joshi, Amrita D</au><au>El Azzouny, Mahmoud</au><au>Wolf, Sonya J</au><au>Obi, Andrea T</au><au>Lipinski, Jay</au><au>Gudjonsson, Johann E</au><au>Xing, Xianying</au><au>Plazyo, Olesya</au><au>Audu, Christopher</au><au>Melvin, William J</au><au>Singer, Kanakadurga</au><au>Henke, Peter K</au><au>Moore, Bethany B</au><au>Burant, Charles</au><au>Kunkel, Steven L</au><au>Gallagher, Katherine A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epigenetic Regulation of TLR4 in Diabetic Macrophages Modulates Immunometabolism and Wound Repair</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2020-05-01</date><risdate>2020</risdate><volume>204</volume><issue>9</issue><spage>2503</spage><epage>2513</epage><pages>2503-2513</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>Macrophages are critical for the initiation and resolution of the inflammatory phase of wound healing. In diabetes, macrophages display a prolonged inflammatory phenotype preventing tissue repair. TLRs, particularly TLR4, have been shown to regulate myeloid-mediated inflammation in wounds. We examined macrophages isolated from wounds of patients afflicted with diabetes and healthy controls as well as a murine diabetic model demonstrating dynamic expression of TLR4 results in altered metabolic pathways in diabetic macrophages. Further, using a myeloid-specific mixed-lineage leukemia 1 (MLL1) knockout (
), we determined that MLL1 drives
expression in diabetic macrophages by regulating levels of histone H3 lysine 4 trimethylation on the
promoter. Mechanistically, MLL1-mediated epigenetic alterations influence diabetic macrophage responsiveness to TLR4 stimulation and inhibit tissue repair. Pharmacological inhibition of the TLR4 pathway using a small molecule inhibitor (TAK-242) as well as genetic depletion of either
(
) or myeloid-specific
resulted in improved diabetic wound healing. These results define an important role for MLL1-mediated epigenetic regulation of TLR4 in pathologic diabetic wound repair and suggest a target for therapeutic manipulation.</abstract><cop>United States</cop><pmid>32205424</pmid><doi>10.4049/jimmunol.1901263</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-9189-5003</orcidid><orcidid>https://orcid.org/0000-0001-7613-2366</orcidid><orcidid>https://orcid.org/0000-0002-3241-5919</orcidid><orcidid>https://orcid.org/0000-0002-6859-7590</orcidid><orcidid>https://orcid.org/0000-0002-5847-8993</orcidid><orcidid>https://orcid.org/0000-0001-8278-3800</orcidid><orcidid>https://orcid.org/0000-0001-9604-0557</orcidid><orcidid>https://orcid.org/0000-0002-0080-0812</orcidid><orcidid>https://orcid.org/0000-0003-3051-745X</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0022-1767 |
| ispartof | The Journal of immunology (1950), 2020-05, Vol.204 (9), p.2503-2513 |
| issn | 0022-1767 1550-6606 |
| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Aged Animals Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - immunology Epigenesis, Genetic - genetics Epigenesis, Genetic - immunology Female Histones - genetics Histones - immunology Humans Inflammation - genetics Inflammation - immunology Inflammation Mediators - immunology Macrophages - immunology Macrophages - physiology Male Mice Mice, Inbred C57BL Mice, Knockout Middle Aged Myeloid-Lymphoid Leukemia Protein - genetics Myeloid-Lymphoid Leukemia Protein - immunology Promoter Regions, Genetic - genetics Promoter Regions, Genetic - immunology Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - immunology Wound Healing - genetics Wound Healing - immunology |
| title | Epigenetic Regulation of TLR4 in Diabetic Macrophages Modulates Immunometabolism and Wound Repair |
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