Interferon activated gene 204 protects against bone loss in experimental periodontitis
Background Periodontal destruction can be the result of different known and yet‐to‐be‐discovered biological pathways. Recent human genetic association studies have implicated interferon‐gamma inducible protein 16 (IFI16) and absent in melanoma 2 (AIM2) with high periodontal interleukin (IL)‐1β level...
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| Veröffentlicht in: | Journal of periodontology (1970) 2022-09, Vol.93 (9), p.1366-1377 |
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| container_title | Journal of periodontology (1970) |
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| creator | Swanson, Karen V. Girnary, Mustafa Alves, Tomaz Ting, Jenny PY Divaris, Kimon Beck, Jim Pucinelli, Carolina Maschietto da Silva, Raquel Assed Bezerra Uyan, Dilek Wilson, Justin E. Seaman, William T. Webster‐Cyriaque, Jennifer Vias, Nishma Jiao, Yizu Cantley, Lloyd Marlier, Arnaud Arnold, Roland R. Marchesan, Julie T. |
| description | Background
Periodontal destruction can be the result of different known and yet‐to‐be‐discovered biological pathways. Recent human genetic association studies have implicated interferon‐gamma inducible protein 16 (IFI16) and absent in melanoma 2 (AIM2) with high periodontal interleukin (IL)‐1β levels and more destructive disease, but mechanistic evidence is lacking. Here, we sought to experimentally validate these observational associations and better understand IFI16 and AIM2's roles in periodontitis.
Methods
Periodontitis was induced in Ifi204–/– (IFI16 murine homolog) and Aim2–/– mice using the ligature model. Chimeric mice were created to identify the main source cells of Ifi204 in the periodontium. IFI16‐silenced human endothelial cells were treated with periodontal pathogens in vitro. Periodontal tissues from Ifi204–/– mice were evaluated for alveolar bone (micro‐CT), cell inflammatory infiltration (MPO+ staining), Il1b (qRT‐PCR), and osteoclast numbers (cathepsin K+ staining).
Results
Ifi204‐deficient mice> exhibited >20% higher alveolar bone loss than wild‐type (WT) (P |
| doi_str_mv | 10.1002/JPER.21-0668 |
| format | Article |
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Periodontal destruction can be the result of different known and yet‐to‐be‐discovered biological pathways. Recent human genetic association studies have implicated interferon‐gamma inducible protein 16 (IFI16) and absent in melanoma 2 (AIM2) with high periodontal interleukin (IL)‐1β levels and more destructive disease, but mechanistic evidence is lacking. Here, we sought to experimentally validate these observational associations and better understand IFI16 and AIM2's roles in periodontitis.
Methods
Periodontitis was induced in Ifi204–/– (IFI16 murine homolog) and Aim2–/– mice using the ligature model. Chimeric mice were created to identify the main source cells of Ifi204 in the periodontium. IFI16‐silenced human endothelial cells were treated with periodontal pathogens in vitro. Periodontal tissues from Ifi204–/– mice were evaluated for alveolar bone (micro‐CT), cell inflammatory infiltration (MPO+ staining), Il1b (qRT‐PCR), and osteoclast numbers (cathepsin K+ staining).
Results
Ifi204‐deficient mice> exhibited >20% higher alveolar bone loss than wild‐type (WT) (P < 0.05), while no significant difference was found in Aim2–/– mice. Ifi204's effect on bone loss was primarily mediated by a nonbone marrow source and was independent of Aim2. Ifi204‐deficient mice had greater neutrophil/macrophage trafficking into gingival tissues regardless of periodontitis development compared to WT. In human endothelial cells, IFI16 decreased the chemokine response to periodontal pathogens. In murine periodontitis, Ifi204 depletion elevated gingival Il1b and increased osteoclast numbers at diseased sites (P < 0.05).
Conclusions
These findings support IFI16's role as a novel regulator of inflammatory cell trafficking to the periodontium that protects against bone loss and offers potential targets for the development of new periodontal disease biomarkers and therapeutics.</description><identifier>ISSN: 0022-3492</identifier><identifier>EISSN: 1943-3670</identifier><identifier>DOI: 10.1002/JPER.21-0668</identifier><identifier>PMID: 35404474</identifier><language>eng</language><publisher>United States</publisher><subject>Alveolar Bone Loss - genetics ; Alveolar Bone Loss - metabolism ; Alveolar Bone Loss - prevention & control ; Animals ; Biomarkers - metabolism ; Cathepsin K ; Disease Models, Animal ; Endothelial Cells - metabolism ; genetics ; host modulation ; inflammasome ; inflammatory disease ; Interferon-gamma - metabolism ; Interferons - metabolism ; Mice ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; periodontitis ; Periodontitis - genetics ; Periodontitis - metabolism ; Phosphoproteins - genetics ; Phosphoproteins - metabolism</subject><ispartof>Journal of periodontology (1970), 2022-09, Vol.93 (9), p.1366-1377</ispartof><rights>2022 American Academy of Periodontology.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3905-1b0039354e345742a8f3882810e8daec3ba53c3cdddcfd6b60546bc068b534fc3</citedby><cites>FETCH-LOGICAL-c3905-1b0039354e345742a8f3882810e8daec3ba53c3cdddcfd6b60546bc068b534fc3</cites><orcidid>0000-0003-0610-3193 ; 0000-0003-3105-0599 ; 0000-0003-1290-7251</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2FJPER.21-0668$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2FJPER.21-0668$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35404474$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Swanson, Karen V.</creatorcontrib><creatorcontrib>Girnary, Mustafa</creatorcontrib><creatorcontrib>Alves, Tomaz</creatorcontrib><creatorcontrib>Ting, Jenny PY</creatorcontrib><creatorcontrib>Divaris, Kimon</creatorcontrib><creatorcontrib>Beck, Jim</creatorcontrib><creatorcontrib>Pucinelli, Carolina Maschietto</creatorcontrib><creatorcontrib>da Silva, Raquel Assed Bezerra</creatorcontrib><creatorcontrib>Uyan, Dilek</creatorcontrib><creatorcontrib>Wilson, Justin E.</creatorcontrib><creatorcontrib>Seaman, William T.</creatorcontrib><creatorcontrib>Webster‐Cyriaque, Jennifer</creatorcontrib><creatorcontrib>Vias, Nishma</creatorcontrib><creatorcontrib>Jiao, Yizu</creatorcontrib><creatorcontrib>Cantley, Lloyd</creatorcontrib><creatorcontrib>Marlier, Arnaud</creatorcontrib><creatorcontrib>Arnold, Roland R.</creatorcontrib><creatorcontrib>Marchesan, Julie T.</creatorcontrib><title>Interferon activated gene 204 protects against bone loss in experimental periodontitis</title><title>Journal of periodontology (1970)</title><addtitle>J Periodontol</addtitle><description>Background
Periodontal destruction can be the result of different known and yet‐to‐be‐discovered biological pathways. Recent human genetic association studies have implicated interferon‐gamma inducible protein 16 (IFI16) and absent in melanoma 2 (AIM2) with high periodontal interleukin (IL)‐1β levels and more destructive disease, but mechanistic evidence is lacking. Here, we sought to experimentally validate these observational associations and better understand IFI16 and AIM2's roles in periodontitis.
Methods
Periodontitis was induced in Ifi204–/– (IFI16 murine homolog) and Aim2–/– mice using the ligature model. Chimeric mice were created to identify the main source cells of Ifi204 in the periodontium. IFI16‐silenced human endothelial cells were treated with periodontal pathogens in vitro. Periodontal tissues from Ifi204–/– mice were evaluated for alveolar bone (micro‐CT), cell inflammatory infiltration (MPO+ staining), Il1b (qRT‐PCR), and osteoclast numbers (cathepsin K+ staining).
Results
Ifi204‐deficient mice> exhibited >20% higher alveolar bone loss than wild‐type (WT) (P < 0.05), while no significant difference was found in Aim2–/– mice. Ifi204's effect on bone loss was primarily mediated by a nonbone marrow source and was independent of Aim2. Ifi204‐deficient mice had greater neutrophil/macrophage trafficking into gingival tissues regardless of periodontitis development compared to WT. In human endothelial cells, IFI16 decreased the chemokine response to periodontal pathogens. In murine periodontitis, Ifi204 depletion elevated gingival Il1b and increased osteoclast numbers at diseased sites (P < 0.05).
Conclusions
These findings support IFI16's role as a novel regulator of inflammatory cell trafficking to the periodontium that protects against bone loss and offers potential targets for the development of new periodontal disease biomarkers and therapeutics.</description><subject>Alveolar Bone Loss - genetics</subject><subject>Alveolar Bone Loss - metabolism</subject><subject>Alveolar Bone Loss - prevention & control</subject><subject>Animals</subject><subject>Biomarkers - metabolism</subject><subject>Cathepsin K</subject><subject>Disease Models, Animal</subject><subject>Endothelial Cells - metabolism</subject><subject>genetics</subject><subject>host modulation</subject><subject>inflammasome</subject><subject>inflammatory disease</subject><subject>Interferon-gamma - metabolism</subject><subject>Interferons - metabolism</subject><subject>Mice</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>periodontitis</subject><subject>Periodontitis - genetics</subject><subject>Periodontitis - metabolism</subject><subject>Phosphoproteins - genetics</subject><subject>Phosphoproteins - metabolism</subject><issn>0022-3492</issn><issn>1943-3670</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUFvVCEUhYmxsWN159qwdNHXAheYx8bENNXWNGlj1C3h8e4bMW9gBKbafy_TqY1uXMHN-XI43EPIK85OOGPi9OPN-acTwTumdf-ELLiR0IFesqdk0WTRgTTikDwv5XsbuQT2jByCkkzKpVyQr5exYp4wp0idr-HWVRzpCiNSwSTd5FTR10LdyoVYKh1SU-ZUCg2R4q8N5rDGWN1Md9c0plhDDeUFOZjcXPDlw3lEvrw__3x20V1df7g8e3fVeTBMdXxgDExLgyDVUgrXT9D3oucM-9Ghh8Ep8ODHcfTTqAfNlNSDZ7ofFMjJwxF5u_fdbIc1jr5FyW62m5bK5TubXLD_KjF8s6t0a43sjRa6Gbx5MMjpxxZLtetQPM6zi5i2xQrd1qcEGNPQ4z3qc_t_xunxGc7srgq7q8IKbndVNPz139Ee4T-7bwDsgZ9hxrv_mt0PnBml4Dd03pWL</recordid><startdate>202209</startdate><enddate>202209</enddate><creator>Swanson, Karen V.</creator><creator>Girnary, Mustafa</creator><creator>Alves, Tomaz</creator><creator>Ting, Jenny PY</creator><creator>Divaris, Kimon</creator><creator>Beck, Jim</creator><creator>Pucinelli, Carolina Maschietto</creator><creator>da Silva, Raquel Assed Bezerra</creator><creator>Uyan, Dilek</creator><creator>Wilson, Justin E.</creator><creator>Seaman, William T.</creator><creator>Webster‐Cyriaque, Jennifer</creator><creator>Vias, Nishma</creator><creator>Jiao, Yizu</creator><creator>Cantley, Lloyd</creator><creator>Marlier, Arnaud</creator><creator>Arnold, Roland R.</creator><creator>Marchesan, Julie T.</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/0000-0003-0610-3193</orcidid><orcidid>https://orcid.org/0000-0003-3105-0599</orcidid><orcidid>https://orcid.org/0000-0003-1290-7251</orcidid></search><sort><creationdate>202209</creationdate><title>Interferon activated gene 204 protects against bone loss in experimental periodontitis</title><author>Swanson, Karen V. ; Girnary, Mustafa ; Alves, Tomaz ; Ting, Jenny PY ; Divaris, Kimon ; Beck, Jim ; Pucinelli, Carolina Maschietto ; da Silva, Raquel Assed Bezerra ; Uyan, Dilek ; Wilson, Justin E. ; Seaman, William T. ; Webster‐Cyriaque, Jennifer ; Vias, Nishma ; Jiao, Yizu ; Cantley, Lloyd ; Marlier, Arnaud ; Arnold, Roland R. ; Marchesan, Julie T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3905-1b0039354e345742a8f3882810e8daec3ba53c3cdddcfd6b60546bc068b534fc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Alveolar Bone Loss - genetics</topic><topic>Alveolar Bone Loss - metabolism</topic><topic>Alveolar Bone Loss - prevention & control</topic><topic>Animals</topic><topic>Biomarkers - metabolism</topic><topic>Cathepsin K</topic><topic>Disease Models, Animal</topic><topic>Endothelial Cells - metabolism</topic><topic>genetics</topic><topic>host modulation</topic><topic>inflammasome</topic><topic>inflammatory disease</topic><topic>Interferon-gamma - metabolism</topic><topic>Interferons - metabolism</topic><topic>Mice</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>periodontitis</topic><topic>Periodontitis - genetics</topic><topic>Periodontitis - metabolism</topic><topic>Phosphoproteins - genetics</topic><topic>Phosphoproteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Swanson, Karen V.</creatorcontrib><creatorcontrib>Girnary, Mustafa</creatorcontrib><creatorcontrib>Alves, Tomaz</creatorcontrib><creatorcontrib>Ting, Jenny PY</creatorcontrib><creatorcontrib>Divaris, Kimon</creatorcontrib><creatorcontrib>Beck, Jim</creatorcontrib><creatorcontrib>Pucinelli, Carolina Maschietto</creatorcontrib><creatorcontrib>da Silva, Raquel Assed Bezerra</creatorcontrib><creatorcontrib>Uyan, Dilek</creatorcontrib><creatorcontrib>Wilson, Justin E.</creatorcontrib><creatorcontrib>Seaman, William T.</creatorcontrib><creatorcontrib>Webster‐Cyriaque, Jennifer</creatorcontrib><creatorcontrib>Vias, Nishma</creatorcontrib><creatorcontrib>Jiao, Yizu</creatorcontrib><creatorcontrib>Cantley, Lloyd</creatorcontrib><creatorcontrib>Marlier, Arnaud</creatorcontrib><creatorcontrib>Arnold, Roland R.</creatorcontrib><creatorcontrib>Marchesan, Julie T.</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>Journal of periodontology (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Swanson, Karen V.</au><au>Girnary, Mustafa</au><au>Alves, Tomaz</au><au>Ting, Jenny PY</au><au>Divaris, Kimon</au><au>Beck, Jim</au><au>Pucinelli, Carolina Maschietto</au><au>da Silva, Raquel Assed Bezerra</au><au>Uyan, Dilek</au><au>Wilson, Justin E.</au><au>Seaman, William T.</au><au>Webster‐Cyriaque, Jennifer</au><au>Vias, Nishma</au><au>Jiao, Yizu</au><au>Cantley, Lloyd</au><au>Marlier, Arnaud</au><au>Arnold, Roland R.</au><au>Marchesan, Julie T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interferon activated gene 204 protects against bone loss in experimental periodontitis</atitle><jtitle>Journal of periodontology (1970)</jtitle><addtitle>J Periodontol</addtitle><date>2022-09</date><risdate>2022</risdate><volume>93</volume><issue>9</issue><spage>1366</spage><epage>1377</epage><pages>1366-1377</pages><issn>0022-3492</issn><eissn>1943-3670</eissn><abstract>Background
Periodontal destruction can be the result of different known and yet‐to‐be‐discovered biological pathways. Recent human genetic association studies have implicated interferon‐gamma inducible protein 16 (IFI16) and absent in melanoma 2 (AIM2) with high periodontal interleukin (IL)‐1β levels and more destructive disease, but mechanistic evidence is lacking. Here, we sought to experimentally validate these observational associations and better understand IFI16 and AIM2's roles in periodontitis.
Methods
Periodontitis was induced in Ifi204–/– (IFI16 murine homolog) and Aim2–/– mice using the ligature model. Chimeric mice were created to identify the main source cells of Ifi204 in the periodontium. IFI16‐silenced human endothelial cells were treated with periodontal pathogens in vitro. Periodontal tissues from Ifi204–/– mice were evaluated for alveolar bone (micro‐CT), cell inflammatory infiltration (MPO+ staining), Il1b (qRT‐PCR), and osteoclast numbers (cathepsin K+ staining).
Results
Ifi204‐deficient mice> exhibited >20% higher alveolar bone loss than wild‐type (WT) (P < 0.05), while no significant difference was found in Aim2–/– mice. Ifi204's effect on bone loss was primarily mediated by a nonbone marrow source and was independent of Aim2. Ifi204‐deficient mice had greater neutrophil/macrophage trafficking into gingival tissues regardless of periodontitis development compared to WT. In human endothelial cells, IFI16 decreased the chemokine response to periodontal pathogens. In murine periodontitis, Ifi204 depletion elevated gingival Il1b and increased osteoclast numbers at diseased sites (P < 0.05).
Conclusions
These findings support IFI16's role as a novel regulator of inflammatory cell trafficking to the periodontium that protects against bone loss and offers potential targets for the development of new periodontal disease biomarkers and therapeutics.</abstract><cop>United States</cop><pmid>35404474</pmid><doi>10.1002/JPER.21-0668</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-0610-3193</orcidid><orcidid>https://orcid.org/0000-0003-3105-0599</orcidid><orcidid>https://orcid.org/0000-0003-1290-7251</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0022-3492 |
| ispartof | Journal of periodontology (1970), 2022-09, Vol.93 (9), p.1366-1377 |
| issn | 0022-3492 1943-3670 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9489626 |
| source | Wiley-Blackwell Journals; MEDLINE |
| subjects | Alveolar Bone Loss - genetics Alveolar Bone Loss - metabolism Alveolar Bone Loss - prevention & control Animals Biomarkers - metabolism Cathepsin K Disease Models, Animal Endothelial Cells - metabolism genetics host modulation inflammasome inflammatory disease Interferon-gamma - metabolism Interferons - metabolism Mice Nuclear Proteins - genetics Nuclear Proteins - metabolism periodontitis Periodontitis - genetics Periodontitis - metabolism Phosphoproteins - genetics Phosphoproteins - metabolism |
| title | Interferon activated gene 204 protects against bone loss in experimental periodontitis |
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