Targeted TNF-α Overexpression Drives Salivary Gland Inflammation
Chronic inflammation of the salivary glands from pathologic conditions such as Sjögren’s syndrome can result in glandular destruction and hyposalivation. To understand which molecular factors may play a role in clinical cases of salivary gland hypofunction, we developed an aquaporin 5 (AQP5) Cre mou...
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| Veröffentlicht in: | Journal of dental research 2019-06, Vol.98 (6), p.713-719 |
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| creator | Limaye, A. Hall, B.E. Zhang, L. Cho, A. Prochazkova, M. Zheng, C. Walker, M. Adewusi, F. Burbelo, P.D. Sun, Z.J. Ambudkar, I.S. Dolan, J.C. Schmidt, B.L. Kulkarni, A.B. |
| description | Chronic inflammation of the salivary glands from pathologic conditions such as Sjögren’s syndrome can result in glandular destruction and hyposalivation. To understand which molecular factors may play a role in clinical cases of salivary gland hypofunction, we developed an aquaporin 5 (AQP5) Cre mouse line to produce genetic recombination predominantly within the acinar cells of the glands. We then bred these mice with the TNF-αglo transgenic line to develop a mouse model with salivary gland–specific overexpression of TNF-α; which replicates conditions seen in sialadenitis, an inflammation of the salivary glands resulting from infection or autoimmune disorders such as Sjögren’s syndrome. The resulting AQP5-Cre/TNF-αglo mice display severe inflammation in the salivary glands with acinar cell atrophy, fibrosis, and dilation of the ducts. AQP5 expression was reduced in the salivary glands, while tight junction integrity appeared to be disrupted. The immune dysregulation in the salivary gland of these mice led to hyposalivation and masticatory dysfunction. |
| doi_str_mv | 10.1177/0022034519837240 |
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To understand which molecular factors may play a role in clinical cases of salivary gland hypofunction, we developed an aquaporin 5 (AQP5) Cre mouse line to produce genetic recombination predominantly within the acinar cells of the glands. We then bred these mice with the TNF-αglo transgenic line to develop a mouse model with salivary gland–specific overexpression of TNF-α; which replicates conditions seen in sialadenitis, an inflammation of the salivary glands resulting from infection or autoimmune disorders such as Sjögren’s syndrome. The resulting AQP5-Cre/TNF-αglo mice display severe inflammation in the salivary glands with acinar cell atrophy, fibrosis, and dilation of the ducts. AQP5 expression was reduced in the salivary glands, while tight junction integrity appeared to be disrupted. The immune dysregulation in the salivary gland of these mice led to hyposalivation and masticatory dysfunction.</description><identifier>ISSN: 0022-0345</identifier><identifier>EISSN: 1544-0591</identifier><identifier>DOI: 10.1177/0022034519837240</identifier><identifier>PMID: 30958728</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject>Acinar cells ; Apoptosis ; Aquaporin 5 ; Atrophy ; Autoimmune diseases ; Biopsy ; Data analysis ; Dentistry ; Fibrosis ; Genetic engineering ; Inflammation ; Mastication ; Polymerase chain reaction ; Recombination ; Research Reports ; Salivary gland ; Sjogren's syndrome ; Transgenic mice ; Tumor necrosis factor-α</subject><ispartof>Journal of dental research, 2019-06, Vol.98 (6), p.713-719</ispartof><rights>International & American Associations for Dental Research 2019</rights><rights>International & American Associations for Dental Research 2019 2019 International & American Associations for Dental Research</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c462t-d8e24c1665a00d4b24f17f45d99e6250e640cc95567101ca3c699e7ef21a1f7d3</citedby><cites>FETCH-LOGICAL-c462t-d8e24c1665a00d4b24f17f45d99e6250e640cc95567101ca3c699e7ef21a1f7d3</cites><orcidid>0000-0001-9049-8807</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/0022034519837240$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/0022034519837240$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>230,314,776,780,881,21798,27901,27902,43597,43598</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30958728$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Limaye, A.</creatorcontrib><creatorcontrib>Hall, B.E.</creatorcontrib><creatorcontrib>Zhang, L.</creatorcontrib><creatorcontrib>Cho, A.</creatorcontrib><creatorcontrib>Prochazkova, M.</creatorcontrib><creatorcontrib>Zheng, C.</creatorcontrib><creatorcontrib>Walker, M.</creatorcontrib><creatorcontrib>Adewusi, F.</creatorcontrib><creatorcontrib>Burbelo, P.D.</creatorcontrib><creatorcontrib>Sun, Z.J.</creatorcontrib><creatorcontrib>Ambudkar, I.S.</creatorcontrib><creatorcontrib>Dolan, J.C.</creatorcontrib><creatorcontrib>Schmidt, B.L.</creatorcontrib><creatorcontrib>Kulkarni, A.B.</creatorcontrib><title>Targeted TNF-α Overexpression Drives Salivary Gland Inflammation</title><title>Journal of dental research</title><addtitle>J Dent Res</addtitle><description>Chronic inflammation of the salivary glands from pathologic conditions such as Sjögren’s syndrome can result in glandular destruction and hyposalivation. To understand which molecular factors may play a role in clinical cases of salivary gland hypofunction, we developed an aquaporin 5 (AQP5) Cre mouse line to produce genetic recombination predominantly within the acinar cells of the glands. We then bred these mice with the TNF-αglo transgenic line to develop a mouse model with salivary gland–specific overexpression of TNF-α; which replicates conditions seen in sialadenitis, an inflammation of the salivary glands resulting from infection or autoimmune disorders such as Sjögren’s syndrome. The resulting AQP5-Cre/TNF-αglo mice display severe inflammation in the salivary glands with acinar cell atrophy, fibrosis, and dilation of the ducts. AQP5 expression was reduced in the salivary glands, while tight junction integrity appeared to be disrupted. The immune dysregulation in the salivary gland of these mice led to hyposalivation and masticatory dysfunction.</description><subject>Acinar cells</subject><subject>Apoptosis</subject><subject>Aquaporin 5</subject><subject>Atrophy</subject><subject>Autoimmune diseases</subject><subject>Biopsy</subject><subject>Data analysis</subject><subject>Dentistry</subject><subject>Fibrosis</subject><subject>Genetic engineering</subject><subject>Inflammation</subject><subject>Mastication</subject><subject>Polymerase chain reaction</subject><subject>Recombination</subject><subject>Research Reports</subject><subject>Salivary gland</subject><subject>Sjogren's syndrome</subject><subject>Transgenic mice</subject><subject>Tumor necrosis factor-α</subject><issn>0022-0345</issn><issn>1544-0591</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp1kc1OwzAQhC0EoqVw54QiceESWDu2E1-QUKEFCcGBcrZcZ1OC8lPstILH4kV4JlyVf4mTD_PteHeGkH0Kx5Sm6QkAY5BwQVWWpIzDBulTwXkMQtFN0l_J8UrvkR3vHwGoYlmyTXoJKJGlLOuTs4lxM-wwjyY3o_jtNbpdosPnuUPvy7aJzl25RB_dmapcGvcSjSvT5NFVU1Smrk0XkF2yVZjK497HOyD3o4vJ8DK-vh1fDc-uY8sl6-I8Q8YtlVIYgJxPGS9oWnCRK4WSCUDJwVolhEwpUGsSK4OSYsGooUWaJwNyuvadL6Y15habzplKz11Zh8V0a0r9W2nKBz1rl1qKRCiWBIOjDwPXPi3Qd7ouvcUqXITtwusQpWQhGcUDevgHfWwXrgnn6UCADOEH1wGBNWVd673D4msZCnrVj_7bTxg5-HnE18BnIQGI14A3M_z-9V_Dd0o7l00</recordid><startdate>20190601</startdate><enddate>20190601</enddate><creator>Limaye, A.</creator><creator>Hall, B.E.</creator><creator>Zhang, L.</creator><creator>Cho, A.</creator><creator>Prochazkova, M.</creator><creator>Zheng, C.</creator><creator>Walker, M.</creator><creator>Adewusi, F.</creator><creator>Burbelo, P.D.</creator><creator>Sun, Z.J.</creator><creator>Ambudkar, I.S.</creator><creator>Dolan, J.C.</creator><creator>Schmidt, B.L.</creator><creator>Kulkarni, A.B.</creator><general>SAGE Publications</general><general>SAGE PUBLICATIONS, INC</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9049-8807</orcidid></search><sort><creationdate>20190601</creationdate><title>Targeted TNF-α Overexpression Drives Salivary Gland Inflammation</title><author>Limaye, A. ; Hall, B.E. ; Zhang, L. ; Cho, A. ; Prochazkova, M. ; Zheng, C. ; Walker, M. ; Adewusi, F. ; Burbelo, P.D. ; Sun, Z.J. ; Ambudkar, I.S. ; Dolan, J.C. ; Schmidt, B.L. ; Kulkarni, A.B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c462t-d8e24c1665a00d4b24f17f45d99e6250e640cc95567101ca3c699e7ef21a1f7d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Acinar cells</topic><topic>Apoptosis</topic><topic>Aquaporin 5</topic><topic>Atrophy</topic><topic>Autoimmune diseases</topic><topic>Biopsy</topic><topic>Data analysis</topic><topic>Dentistry</topic><topic>Fibrosis</topic><topic>Genetic engineering</topic><topic>Inflammation</topic><topic>Mastication</topic><topic>Polymerase chain reaction</topic><topic>Recombination</topic><topic>Research Reports</topic><topic>Salivary gland</topic><topic>Sjogren's syndrome</topic><topic>Transgenic mice</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Limaye, A.</creatorcontrib><creatorcontrib>Hall, B.E.</creatorcontrib><creatorcontrib>Zhang, L.</creatorcontrib><creatorcontrib>Cho, A.</creatorcontrib><creatorcontrib>Prochazkova, M.</creatorcontrib><creatorcontrib>Zheng, C.</creatorcontrib><creatorcontrib>Walker, M.</creatorcontrib><creatorcontrib>Adewusi, F.</creatorcontrib><creatorcontrib>Burbelo, P.D.</creatorcontrib><creatorcontrib>Sun, Z.J.</creatorcontrib><creatorcontrib>Ambudkar, I.S.</creatorcontrib><creatorcontrib>Dolan, J.C.</creatorcontrib><creatorcontrib>Schmidt, B.L.</creatorcontrib><creatorcontrib>Kulkarni, A.B.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of dental research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Limaye, A.</au><au>Hall, B.E.</au><au>Zhang, L.</au><au>Cho, A.</au><au>Prochazkova, M.</au><au>Zheng, C.</au><au>Walker, M.</au><au>Adewusi, F.</au><au>Burbelo, P.D.</au><au>Sun, Z.J.</au><au>Ambudkar, I.S.</au><au>Dolan, J.C.</au><au>Schmidt, B.L.</au><au>Kulkarni, A.B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeted TNF-α Overexpression Drives Salivary Gland Inflammation</atitle><jtitle>Journal of dental research</jtitle><addtitle>J Dent Res</addtitle><date>2019-06-01</date><risdate>2019</risdate><volume>98</volume><issue>6</issue><spage>713</spage><epage>719</epage><pages>713-719</pages><issn>0022-0345</issn><eissn>1544-0591</eissn><abstract>Chronic inflammation of the salivary glands from pathologic conditions such as Sjögren’s syndrome can result in glandular destruction and hyposalivation. To understand which molecular factors may play a role in clinical cases of salivary gland hypofunction, we developed an aquaporin 5 (AQP5) Cre mouse line to produce genetic recombination predominantly within the acinar cells of the glands. We then bred these mice with the TNF-αglo transgenic line to develop a mouse model with salivary gland–specific overexpression of TNF-α; which replicates conditions seen in sialadenitis, an inflammation of the salivary glands resulting from infection or autoimmune disorders such as Sjögren’s syndrome. The resulting AQP5-Cre/TNF-αglo mice display severe inflammation in the salivary glands with acinar cell atrophy, fibrosis, and dilation of the ducts. AQP5 expression was reduced in the salivary glands, while tight junction integrity appeared to be disrupted. 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| subjects | Acinar cells Apoptosis Aquaporin 5 Atrophy Autoimmune diseases Biopsy Data analysis Dentistry Fibrosis Genetic engineering Inflammation Mastication Polymerase chain reaction Recombination Research Reports Salivary gland Sjogren's syndrome Transgenic mice Tumor necrosis factor-α |
| title | Targeted TNF-α Overexpression Drives Salivary Gland Inflammation |
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