Epithelial Cell Apoptosis in Recurrent Aphthous Ulcers
A recurrent aphthous ulcer (RAU) is a common inflammatory ulcerative lesion affecting oral mucosa. We studied the eventual apoptosis of epithelial cells from the point of view of ulcer and inflammation. RAU lesions and healthy mucosa samples were immunostained for caspase-3 and high-mobility group b...
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description | A recurrent aphthous ulcer (RAU) is a common inflammatory ulcerative lesion affecting oral mucosa. We studied the eventual apoptosis of epithelial cells from the point of view of ulcer and inflammation. RAU lesions and healthy mucosa samples were immunostained for caspase-3 and high-mobility group box 1 (HMGB1). DNA nicks were identified using TUNEL staining. We studied the effects of tumor necrosis factor α (TNFα) and interferon γ (IFNγ) on the toll-like receptor 2 and 4 (TLR2 and TLR4) expression of human oral SCC-25 keratinocytes. We also studied the effects of self-DNA, all-thiol-HMGB1, and disulfide-HMGB1 on epithelial cells, with or without IFNγ. At the edge of RAU lesions, all epithelial cell layers were caspase-3+, TUNEL+, and HMGB-1+ and had widened intercellular spaces. In contrast, healthy epithelial cells were negative for caspase-3 and TUNEL staining. HMGB1 was seen in only the basal cell layers, and the cells retained close cell-to-cell contacts. Self-DNA increased TNF-α mRNA (P = 0.02) in SCC-25 cells. Both TNFα and IFNγ (P = 0.01) increased TLR2. Upon TNFα stimulation, SCC-25 cells lost their nuclear HMGB1 staining. HMGB1 did not increase IL-8, IL-6, or TNF-α mRNA in SCC-25 cells, which was unaffected by the presence of IFNγ. We conclude that in healthy epithelium, the most superficial cells at the end of their life cycle are simply desquamated. In contrast, RAU is characterized by top-to-bottom apoptosis such that dead cells may slough off, leading to an ulcer. Because of a lack of scavenging anti-inflammatory macrophages, apoptotic cells probably undergo secondary necrosis releasing proinflammatory danger signals, which may contribute to the peripheral inflammatory halo. This is supported by self-DNA-induced TNFα synthesis. In contrast to TLR4- and TLR2-binding lipopolysaccharide used as a positive control, disulfide-HMGB1 did not stimulate proinflammatory cytokines. |
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We studied the eventual apoptosis of epithelial cells from the point of view of ulcer and inflammation. RAU lesions and healthy mucosa samples were immunostained for caspase-3 and high-mobility group box 1 (HMGB1). DNA nicks were identified using TUNEL staining. We studied the effects of tumor necrosis factor α (TNFα) and interferon γ (IFNγ) on the toll-like receptor 2 and 4 (TLR2 and TLR4) expression of human oral SCC-25 keratinocytes. We also studied the effects of self-DNA, all-thiol-HMGB1, and disulfide-HMGB1 on epithelial cells, with or without IFNγ. At the edge of RAU lesions, all epithelial cell layers were caspase-3+, TUNEL+, and HMGB-1+ and had widened intercellular spaces. In contrast, healthy epithelial cells were negative for caspase-3 and TUNEL staining. HMGB1 was seen in only the basal cell layers, and the cells retained close cell-to-cell contacts. Self-DNA increased TNF-α mRNA (P = 0.02) in SCC-25 cells. Both TNFα and IFNγ (P = 0.01) increased TLR2. Upon TNFα stimulation, SCC-25 cells lost their nuclear HMGB1 staining. HMGB1 did not increase IL-8, IL-6, or TNF-α mRNA in SCC-25 cells, which was unaffected by the presence of IFNγ. We conclude that in healthy epithelium, the most superficial cells at the end of their life cycle are simply desquamated. In contrast, RAU is characterized by top-to-bottom apoptosis such that dead cells may slough off, leading to an ulcer. Because of a lack of scavenging anti-inflammatory macrophages, apoptotic cells probably undergo secondary necrosis releasing proinflammatory danger signals, which may contribute to the peripheral inflammatory halo. This is supported by self-DNA-induced TNFα synthesis. In contrast to TLR4- and TLR2-binding lipopolysaccharide used as a positive control, disulfide-HMGB1 did not stimulate proinflammatory cytokines.</description><identifier>ISSN: 0022-0345</identifier><identifier>EISSN: 1544-0591</identifier><identifier>DOI: 10.1177/0022034515581012</identifier><identifier>PMID: 25861801</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject>Adult ; Aged ; Apoptosis ; Apoptosis - physiology ; Biopsy ; Caspase ; Caspase 3 - analysis ; Caspase-3 ; Cell Culture Techniques ; Cell Line ; Cell Nucleus - ultrastructure ; Cytokines ; Dentistry ; Deoxyribonucleic acid ; DNA ; DNA biosynthesis ; Epithelial cells ; Epithelial Cells - drug effects ; Epithelial Cells - pathology ; Epithelium ; Extracellular Space ; Fibroblasts ; HMGB1 protein ; HMGB1 Protein - analysis ; HMGB1 Protein - pharmacology ; Humans ; Immunohistochemistry ; In Situ Nick-End Labeling ; Inflammation ; Inflammation Mediators - analysis ; Interferon-gamma - pharmacology ; Interleukin 6 ; Interleukin 8 ; Interleukin-6 - analysis ; Interleukin-8 - analysis ; Interleukin-8 - drug effects ; Keratinocytes ; Keratinocytes - drug effects ; Keratinocytes - pathology ; Lesions ; Life cycles ; Lipopolysaccharides ; Macrophages ; Middle Aged ; Mouth Mucosa - pathology ; mRNA ; Mucosa ; Penicillin ; Stomatitis, Aphthous - pathology ; TLR2 protein ; TLR4 protein ; Toll-Like Receptor 2 - drug effects ; Toll-Like Receptor 4 - drug effects ; Toll-like receptors ; Tumor Necrosis Factor-alpha - pharmacology ; Tumor necrosis factor-α ; Ulcers ; Young Adult ; γ-Interferon</subject><ispartof>Journal of dental research, 2015-07, Vol.94 (7), p.928-935</ispartof><rights>International & American Associations for Dental Research 2015</rights><rights>International & American Associations for Dental Research 2015.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c365t-dd4cf7863cf3febef71d7f9f4551d0794350cd3705e1d854754c81087e07d6243</citedby><cites>FETCH-LOGICAL-c365t-dd4cf7863cf3febef71d7f9f4551d0794350cd3705e1d854754c81087e07d6243</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/0022034515581012$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/0022034515581012$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,778,782,21802,27907,27908,43604,43605</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25861801$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Al-Samadi, A.</creatorcontrib><creatorcontrib>Drozd, A.</creatorcontrib><creatorcontrib>Salem, A.</creatorcontrib><creatorcontrib>Hietanen, J.</creatorcontrib><creatorcontrib>Häyrinen-Immonen, R.</creatorcontrib><creatorcontrib>Konttinen, Y.T.</creatorcontrib><title>Epithelial Cell Apoptosis in Recurrent Aphthous Ulcers</title><title>Journal of dental research</title><addtitle>J Dent Res</addtitle><description>A recurrent aphthous ulcer (RAU) is a common inflammatory ulcerative lesion affecting oral mucosa. We studied the eventual apoptosis of epithelial cells from the point of view of ulcer and inflammation. RAU lesions and healthy mucosa samples were immunostained for caspase-3 and high-mobility group box 1 (HMGB1). DNA nicks were identified using TUNEL staining. We studied the effects of tumor necrosis factor α (TNFα) and interferon γ (IFNγ) on the toll-like receptor 2 and 4 (TLR2 and TLR4) expression of human oral SCC-25 keratinocytes. We also studied the effects of self-DNA, all-thiol-HMGB1, and disulfide-HMGB1 on epithelial cells, with or without IFNγ. At the edge of RAU lesions, all epithelial cell layers were caspase-3+, TUNEL+, and HMGB-1+ and had widened intercellular spaces. In contrast, healthy epithelial cells were negative for caspase-3 and TUNEL staining. HMGB1 was seen in only the basal cell layers, and the cells retained close cell-to-cell contacts. Self-DNA increased TNF-α mRNA (P = 0.02) in SCC-25 cells. Both TNFα and IFNγ (P = 0.01) increased TLR2. Upon TNFα stimulation, SCC-25 cells lost their nuclear HMGB1 staining. HMGB1 did not increase IL-8, IL-6, or TNF-α mRNA in SCC-25 cells, which was unaffected by the presence of IFNγ. We conclude that in healthy epithelium, the most superficial cells at the end of their life cycle are simply desquamated. In contrast, RAU is characterized by top-to-bottom apoptosis such that dead cells may slough off, leading to an ulcer. Because of a lack of scavenging anti-inflammatory macrophages, apoptotic cells probably undergo secondary necrosis releasing proinflammatory danger signals, which may contribute to the peripheral inflammatory halo. This is supported by self-DNA-induced TNFα synthesis. In contrast to TLR4- and TLR2-binding lipopolysaccharide used as a positive control, disulfide-HMGB1 did not stimulate proinflammatory cytokines.</description><subject>Adult</subject><subject>Aged</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Biopsy</subject><subject>Caspase</subject><subject>Caspase 3 - analysis</subject><subject>Caspase-3</subject><subject>Cell Culture Techniques</subject><subject>Cell Line</subject><subject>Cell Nucleus - ultrastructure</subject><subject>Cytokines</subject><subject>Dentistry</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA biosynthesis</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - pathology</subject><subject>Epithelium</subject><subject>Extracellular Space</subject><subject>Fibroblasts</subject><subject>HMGB1 protein</subject><subject>HMGB1 Protein - analysis</subject><subject>HMGB1 Protein - pharmacology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>In Situ Nick-End Labeling</subject><subject>Inflammation</subject><subject>Inflammation Mediators - analysis</subject><subject>Interferon-gamma - pharmacology</subject><subject>Interleukin 6</subject><subject>Interleukin 8</subject><subject>Interleukin-6 - analysis</subject><subject>Interleukin-8 - analysis</subject><subject>Interleukin-8 - drug effects</subject><subject>Keratinocytes</subject><subject>Keratinocytes - drug effects</subject><subject>Keratinocytes - pathology</subject><subject>Lesions</subject><subject>Life cycles</subject><subject>Lipopolysaccharides</subject><subject>Macrophages</subject><subject>Middle Aged</subject><subject>Mouth Mucosa - pathology</subject><subject>mRNA</subject><subject>Mucosa</subject><subject>Penicillin</subject><subject>Stomatitis, Aphthous - pathology</subject><subject>TLR2 protein</subject><subject>TLR4 protein</subject><subject>Toll-Like Receptor 2 - drug effects</subject><subject>Toll-Like Receptor 4 - drug effects</subject><subject>Toll-like receptors</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumor necrosis factor-α</subject><subject>Ulcers</subject><subject>Young Adult</subject><subject>γ-Interferon</subject><issn>0022-0345</issn><issn>1544-0591</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtLw0AQxhdRbK3ePUnAi5fozD6ym2Mp9QEFQew5pPuwKWkTd5OD_70bWhUKngZmfvPNNx8h1wj3iFI-AFAKjAsUQiEgPSFjFJynIHI8JeNhnA7zEbkIYQOAOVXsnIyoUBkqwDHJ5m3VrW1dlXUys3WdTNum7ZpQhaTaJW9W997bXRfb627d9CFZ1tr6cEnOXFkHe3WoE7J8nL_PntPF69PLbLpINctElxrDtZMqY9oxZ1fWSTTS5Y4LgQZkzpkAbZgEYdEowaXgOj6ipAVpMsrZhNztdVvffPY2dMW2Cjr6LHc2uikwy4e_lVARvT1CN03vd9FdQRlABlIpGinYU9o3IXjritZX29J_FQjFkGlxnGlcuTkI96utNb8LPyFGIN0Dofywf1f_FfwG-FB7PQ</recordid><startdate>20150701</startdate><enddate>20150701</enddate><creator>Al-Samadi, A.</creator><creator>Drozd, A.</creator><creator>Salem, A.</creator><creator>Hietanen, J.</creator><creator>Häyrinen-Immonen, R.</creator><creator>Konttinen, Y.T.</creator><general>SAGE Publications</general><general>SAGE PUBLICATIONS, INC</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>U9A</scope><scope>7X8</scope></search><sort><creationdate>20150701</creationdate><title>Epithelial Cell Apoptosis in Recurrent Aphthous Ulcers</title><author>Al-Samadi, A. ; Drozd, A. ; Salem, A. ; Hietanen, J. ; Häyrinen-Immonen, R. ; Konttinen, Y.T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c365t-dd4cf7863cf3febef71d7f9f4551d0794350cd3705e1d854754c81087e07d6243</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Apoptosis</topic><topic>Apoptosis - physiology</topic><topic>Biopsy</topic><topic>Caspase</topic><topic>Caspase 3 - analysis</topic><topic>Caspase-3</topic><topic>Cell Culture Techniques</topic><topic>Cell Line</topic><topic>Cell Nucleus - ultrastructure</topic><topic>Cytokines</topic><topic>Dentistry</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA biosynthesis</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - pathology</topic><topic>Epithelium</topic><topic>Extracellular Space</topic><topic>Fibroblasts</topic><topic>HMGB1 protein</topic><topic>HMGB1 Protein - analysis</topic><topic>HMGB1 Protein - pharmacology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>In Situ Nick-End Labeling</topic><topic>Inflammation</topic><topic>Inflammation Mediators - analysis</topic><topic>Interferon-gamma - pharmacology</topic><topic>Interleukin 6</topic><topic>Interleukin 8</topic><topic>Interleukin-6 - analysis</topic><topic>Interleukin-8 - analysis</topic><topic>Interleukin-8 - drug effects</topic><topic>Keratinocytes</topic><topic>Keratinocytes - drug effects</topic><topic>Keratinocytes - pathology</topic><topic>Lesions</topic><topic>Life cycles</topic><topic>Lipopolysaccharides</topic><topic>Macrophages</topic><topic>Middle Aged</topic><topic>Mouth Mucosa - pathology</topic><topic>mRNA</topic><topic>Mucosa</topic><topic>Penicillin</topic><topic>Stomatitis, Aphthous - pathology</topic><topic>TLR2 protein</topic><topic>TLR4 protein</topic><topic>Toll-Like Receptor 2 - drug effects</topic><topic>Toll-Like Receptor 4 - drug effects</topic><topic>Toll-like receptors</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Tumor necrosis factor-α</topic><topic>Ulcers</topic><topic>Young Adult</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Al-Samadi, A.</creatorcontrib><creatorcontrib>Drozd, A.</creatorcontrib><creatorcontrib>Salem, A.</creatorcontrib><creatorcontrib>Hietanen, J.</creatorcontrib><creatorcontrib>Häyrinen-Immonen, R.</creatorcontrib><creatorcontrib>Konttinen, Y.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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of dental research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Al-Samadi, A.</au><au>Drozd, A.</au><au>Salem, A.</au><au>Hietanen, J.</au><au>Häyrinen-Immonen, R.</au><au>Konttinen, Y.T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epithelial Cell Apoptosis in Recurrent Aphthous Ulcers</atitle><jtitle>Journal of dental research</jtitle><addtitle>J Dent Res</addtitle><date>2015-07-01</date><risdate>2015</risdate><volume>94</volume><issue>7</issue><spage>928</spage><epage>935</epage><pages>928-935</pages><issn>0022-0345</issn><eissn>1544-0591</eissn><abstract>A recurrent aphthous ulcer (RAU) is a common inflammatory ulcerative lesion affecting oral mucosa. We studied the eventual apoptosis of epithelial cells from the point of view of ulcer and inflammation. RAU lesions and healthy mucosa samples were immunostained for caspase-3 and high-mobility group box 1 (HMGB1). DNA nicks were identified using TUNEL staining. We studied the effects of tumor necrosis factor α (TNFα) and interferon γ (IFNγ) on the toll-like receptor 2 and 4 (TLR2 and TLR4) expression of human oral SCC-25 keratinocytes. We also studied the effects of self-DNA, all-thiol-HMGB1, and disulfide-HMGB1 on epithelial cells, with or without IFNγ. At the edge of RAU lesions, all epithelial cell layers were caspase-3+, TUNEL+, and HMGB-1+ and had widened intercellular spaces. In contrast, healthy epithelial cells were negative for caspase-3 and TUNEL staining. HMGB1 was seen in only the basal cell layers, and the cells retained close cell-to-cell contacts. Self-DNA increased TNF-α mRNA (P = 0.02) in SCC-25 cells. Both TNFα and IFNγ (P = 0.01) increased TLR2. Upon TNFα stimulation, SCC-25 cells lost their nuclear HMGB1 staining. HMGB1 did not increase IL-8, IL-6, or TNF-α mRNA in SCC-25 cells, which was unaffected by the presence of IFNγ. We conclude that in healthy epithelium, the most superficial cells at the end of their life cycle are simply desquamated. In contrast, RAU is characterized by top-to-bottom apoptosis such that dead cells may slough off, leading to an ulcer. Because of a lack of scavenging anti-inflammatory macrophages, apoptotic cells probably undergo secondary necrosis releasing proinflammatory danger signals, which may contribute to the peripheral inflammatory halo. This is supported by self-DNA-induced TNFα synthesis. In contrast to TLR4- and TLR2-binding lipopolysaccharide used as a positive control, disulfide-HMGB1 did not stimulate proinflammatory cytokines.</abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><pmid>25861801</pmid><doi>10.1177/0022034515581012</doi><tpages>8</tpages></addata></record> |
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subjects | Adult Aged Apoptosis Apoptosis - physiology Biopsy Caspase Caspase 3 - analysis Caspase-3 Cell Culture Techniques Cell Line Cell Nucleus - ultrastructure Cytokines Dentistry Deoxyribonucleic acid DNA DNA biosynthesis Epithelial cells Epithelial Cells - drug effects Epithelial Cells - pathology Epithelium Extracellular Space Fibroblasts HMGB1 protein HMGB1 Protein - analysis HMGB1 Protein - pharmacology Humans Immunohistochemistry In Situ Nick-End Labeling Inflammation Inflammation Mediators - analysis Interferon-gamma - pharmacology Interleukin 6 Interleukin 8 Interleukin-6 - analysis Interleukin-8 - analysis Interleukin-8 - drug effects Keratinocytes Keratinocytes - drug effects Keratinocytes - pathology Lesions Life cycles Lipopolysaccharides Macrophages Middle Aged Mouth Mucosa - pathology mRNA Mucosa Penicillin Stomatitis, Aphthous - pathology TLR2 protein TLR4 protein Toll-Like Receptor 2 - drug effects Toll-Like Receptor 4 - drug effects Toll-like receptors Tumor Necrosis Factor-alpha - pharmacology Tumor necrosis factor-α Ulcers Young Adult γ-Interferon |
title | Epithelial Cell Apoptosis in Recurrent Aphthous Ulcers |
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