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Age-associated Inflammatory Changes: Role of Nutritional Intervention
Accumulating evidence suggests that aging is associated with dysregulated immune and inflammatory responses. Investigation into the cellular and molecular mechanisms underlying this phenomenon suggests that an up-regulated cyclooxygenase (COX)-2 expression, and resulting increase in production of pr...
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| Published in: | Nutrition reviews 2007-12, Vol.65 (12), p.S213-S216 |
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| Language: | English |
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| container_end_page | S216 |
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| container_title | Nutrition reviews |
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| creator | Meydani, S.N Wu, D |
| description | Accumulating evidence suggests that aging is associated with dysregulated immune and inflammatory responses. Investigation into the cellular and molecular mechanisms underlying this phenomenon suggests that an up-regulated cyclooxygenase (COX)-2 expression, and resulting increase in production of prostaglandin E2 (PGE2), is a critical factor. Macrophages from old mice have significantly higher levels of PGE2 production compared with those from young mice, a result of increased COX-2 expression and protein levels leading to increased COX enzyme activity. Further, it is possible that the age-associated increase in macro-phage PGE2 production is due to ceramide-induced up-regulation of nuclear factor-kappa B activation. Such processes may also occur in cell types other than macrophages, lending further insight into potential mechanisms of age-related disease. More research is necessary to determine the efficacy of nutrient/dietary modifications, such as antioxidants and lipids, for reducing the age-related increase in COX activity and PGE2 production that are associated with several disease states. |
| doi_str_mv | 10.1111/j.1753-4887.2007.tb00365.x |
| format | article |
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Investigation into the cellular and molecular mechanisms underlying this phenomenon suggests that an up-regulated cyclooxygenase (COX)-2 expression, and resulting increase in production of prostaglandin E2 (PGE2), is a critical factor. Macrophages from old mice have significantly higher levels of PGE2 production compared with those from young mice, a result of increased COX-2 expression and protein levels leading to increased COX enzyme activity. Further, it is possible that the age-associated increase in macro-phage PGE2 production is due to ceramide-induced up-regulation of nuclear factor-kappa B activation. Such processes may also occur in cell types other than macrophages, lending further insight into potential mechanisms of age-related disease. More research is necessary to determine the efficacy of nutrient/dietary modifications, such as antioxidants and lipids, for reducing the age-related increase in COX activity and PGE2 production that are associated with several disease states.</description><identifier>ISSN: 0029-6643</identifier><identifier>EISSN: 1753-4887</identifier><identifier>DOI: 10.1111/j.1753-4887.2007.tb00365.x</identifier><identifier>PMID: 18240551</identifier><identifier>CODEN: NUREA8</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Age ; Aged ; Aged, 80 and over ; Aging ; Aging - physiology ; Alzheimer's disease ; amides ; biochemical mechanisms ; Biological and medical sciences ; ceramide ; cyclooxygenase 2 ; Cyclooxygenase 2 - metabolism ; Diet ; Dinoprostone - metabolism ; elderly ; elderly nutrition ; enzyme activity ; Fundamental and applied biological sciences. Psychology ; human health ; human physiology ; Humans ; Immune system ; immunity ; Infectious diseases ; Inflammation ; Inflammation - enzymology ; inflammatory response ; literature reviews ; macrophages ; Molecular and cellular biology ; Mortality ; nuclear factor-kappa B ; nutritional intervention ; pathogenesis ; prostaglandin E2 ; prostaglandin synthase ; prostaglandins ; risk factors ; senescence ; sphingomyelinase ; Studies ; Vitamin E</subject><ispartof>Nutrition reviews, 2007-12, Vol.65 (12), p.S213-S216</ispartof><rights>2008 INIST-CNRS</rights><rights>Copyright International Life Sciences Institute Dec 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4083-f0985ca7864566e1f84db18e0de0c35ad6d6e6004dcaf83de114586c360a00f43</citedby><cites>FETCH-LOGICAL-c4083-f0985ca7864566e1f84db18e0de0c35ad6d6e6004dcaf83de114586c360a00f43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>310,311,315,786,790,795,796,23958,23959,25170,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20040450$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18240551$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Meydani, S.N</creatorcontrib><creatorcontrib>Wu, D</creatorcontrib><title>Age-associated Inflammatory Changes: Role of Nutritional Intervention</title><title>Nutrition reviews</title><addtitle>Nutr Rev</addtitle><description>Accumulating evidence suggests that aging is associated with dysregulated immune and inflammatory responses. Investigation into the cellular and molecular mechanisms underlying this phenomenon suggests that an up-regulated cyclooxygenase (COX)-2 expression, and resulting increase in production of prostaglandin E2 (PGE2), is a critical factor. Macrophages from old mice have significantly higher levels of PGE2 production compared with those from young mice, a result of increased COX-2 expression and protein levels leading to increased COX enzyme activity. Further, it is possible that the age-associated increase in macro-phage PGE2 production is due to ceramide-induced up-regulation of nuclear factor-kappa B activation. Such processes may also occur in cell types other than macrophages, lending further insight into potential mechanisms of age-related disease. More research is necessary to determine the efficacy of nutrient/dietary modifications, such as antioxidants and lipids, for reducing the age-related increase in COX activity and PGE2 production that are associated with several disease states.</description><subject>Age</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aging</subject><subject>Aging - physiology</subject><subject>Alzheimer's disease</subject><subject>amides</subject><subject>biochemical mechanisms</subject><subject>Biological and medical sciences</subject><subject>ceramide</subject><subject>cyclooxygenase 2</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Diet</subject><subject>Dinoprostone - metabolism</subject><subject>elderly</subject><subject>elderly nutrition</subject><subject>enzyme activity</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>human health</subject><subject>human physiology</subject><subject>Humans</subject><subject>Immune system</subject><subject>immunity</subject><subject>Infectious diseases</subject><subject>Inflammation</subject><subject>Inflammation - enzymology</subject><subject>inflammatory response</subject><subject>literature reviews</subject><subject>macrophages</subject><subject>Molecular and cellular biology</subject><subject>Mortality</subject><subject>nuclear factor-kappa B</subject><subject>nutritional intervention</subject><subject>pathogenesis</subject><subject>prostaglandin E2</subject><subject>prostaglandin synthase</subject><subject>prostaglandins</subject><subject>risk factors</subject><subject>senescence</subject><subject>sphingomyelinase</subject><subject>Studies</subject><subject>Vitamin E</subject><issn>0029-6643</issn><issn>1753-4887</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNqVkF1v0zAUhi0EYmXwF6CaBHcJx_FHnF0xqm4MRhEbFZeW69glXRIPO4H23-MoUZG4wzeW5ee8fv0gdIYhxXG93aU4ZyShQuRpBpCn3QaAcJbuH6HZ8eoxmgFkRcI5JSfoWQg7AMBZQZ6iEywyCozhGVpebE2iQnC6Up0p59etrVXTqM75w3zxQ7VbE87nt642c2fnq77zVVe5VtWR7Iz_Zdrh-Bw9saoO5sW0n6L15fLb4kNy8-XqenFxk2gKgiQWCsG0ygWnjHODraDlBgsDpQFNmCp5yQ0HoKVWVpDSYEyZ4JpwUACWklP0Zsx98O5nb0InmypoU9eqNa4PMo82BMmLCJ79A-5c72PtIDOckfh1wBE6HyHtXQjeWPngq0b5g8QgB9NyJwedctApB9NyMi33cfjl9EK_aUz5d3RSG4HXE6CCVrX1qtVVOHIxjgJlELl3I_e7qs3hPyrI1fp2eZdhEiOSMaIKndkfI5S_lzwnOZPfV1fyEhefss8fv8r3kX818lY5qbY-1lrfZdEIQAGYUkH-AO-tslU</recordid><startdate>200712</startdate><enddate>200712</enddate><creator>Meydani, S.N</creator><creator>Wu, D</creator><general>Blackwell Publishing Ltd</general><general>International Life Sciences Institute</general><general>Oxford University Press</general><scope>FBQ</scope><scope>BSCLL</scope><scope>IQODW</scope><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>3V.</scope><scope>7RV</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0K</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>200712</creationdate><title>Age-associated Inflammatory Changes: Role of Nutritional Intervention</title><author>Meydani, S.N ; Wu, D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4083-f0985ca7864566e1f84db18e0de0c35ad6d6e6004dcaf83de114586c360a00f43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Age</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aging</topic><topic>Aging - physiology</topic><topic>Alzheimer's disease</topic><topic>amides</topic><topic>biochemical mechanisms</topic><topic>Biological and medical sciences</topic><topic>ceramide</topic><topic>cyclooxygenase 2</topic><topic>Cyclooxygenase 2 - metabolism</topic><topic>Diet</topic><topic>Dinoprostone - metabolism</topic><topic>elderly</topic><topic>elderly nutrition</topic><topic>enzyme activity</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>human health</topic><topic>human physiology</topic><topic>Humans</topic><topic>Immune system</topic><topic>immunity</topic><topic>Infectious diseases</topic><topic>Inflammation</topic><topic>Inflammation - enzymology</topic><topic>inflammatory response</topic><topic>literature reviews</topic><topic>macrophages</topic><topic>Molecular and cellular biology</topic><topic>Mortality</topic><topic>nuclear factor-kappa B</topic><topic>nutritional intervention</topic><topic>pathogenesis</topic><topic>prostaglandin E2</topic><topic>prostaglandin synthase</topic><topic>prostaglandins</topic><topic>risk factors</topic><topic>senescence</topic><topic>sphingomyelinase</topic><topic>Studies</topic><topic>Vitamin E</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Meydani, S.N</creatorcontrib><creatorcontrib>Wu, D</creatorcontrib><collection>AGRIS</collection><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>Agricultural Science Collection</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Agriculture Science Database</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Research Library</collection><collection>Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>Nutrition reviews</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Meydani, S.N</au><au>Wu, D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Age-associated Inflammatory Changes: Role of Nutritional Intervention</atitle><jtitle>Nutrition reviews</jtitle><addtitle>Nutr Rev</addtitle><date>2007-12</date><risdate>2007</risdate><volume>65</volume><issue>12</issue><spage>S213</spage><epage>S216</epage><pages>S213-S216</pages><issn>0029-6643</issn><eissn>1753-4887</eissn><coden>NUREA8</coden><notes>http://hdl.handle.net/10113/18308</notes><notes>ArticleID:NURES213</notes><notes>ark:/67375/WNG-F19K2MJQ-B</notes><notes>istex:FC50222AA64D076985C7A7DB46E573852CFFCB3B</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-3</notes><notes>content type line 23</notes><notes>ObjectType-Review-2</notes><abstract>Accumulating evidence suggests that aging is associated with dysregulated immune and inflammatory responses. Investigation into the cellular and molecular mechanisms underlying this phenomenon suggests that an up-regulated cyclooxygenase (COX)-2 expression, and resulting increase in production of prostaglandin E2 (PGE2), is a critical factor. Macrophages from old mice have significantly higher levels of PGE2 production compared with those from young mice, a result of increased COX-2 expression and protein levels leading to increased COX enzyme activity. Further, it is possible that the age-associated increase in macro-phage PGE2 production is due to ceramide-induced up-regulation of nuclear factor-kappa B activation. Such processes may also occur in cell types other than macrophages, lending further insight into potential mechanisms of age-related disease. More research is necessary to determine the efficacy of nutrient/dietary modifications, such as antioxidants and lipids, for reducing the age-related increase in COX activity and PGE2 production that are associated with several disease states.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>18240551</pmid><doi>10.1111/j.1753-4887.2007.tb00365.x</doi><tpages>4</tpages></addata></record> |
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| identifier | ISSN: 0029-6643 |
| ispartof | Nutrition reviews, 2007-12, Vol.65 (12), p.S213-S216 |
| issn | 0029-6643 1753-4887 |
| language | eng |
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| source | Oxford Academic Journals (OUP) |
| subjects | Age Aged Aged, 80 and over Aging Aging - physiology Alzheimer's disease amides biochemical mechanisms Biological and medical sciences ceramide cyclooxygenase 2 Cyclooxygenase 2 - metabolism Diet Dinoprostone - metabolism elderly elderly nutrition enzyme activity Fundamental and applied biological sciences. Psychology human health human physiology Humans Immune system immunity Infectious diseases Inflammation Inflammation - enzymology inflammatory response literature reviews macrophages Molecular and cellular biology Mortality nuclear factor-kappa B nutritional intervention pathogenesis prostaglandin E2 prostaglandin synthase prostaglandins risk factors senescence sphingomyelinase Studies Vitamin E |
| title | Age-associated Inflammatory Changes: Role of Nutritional Intervention |
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