Pro- and Anti-Inflammatory Factors Cooperate to Control Hyaluronan Synthesis in Lung Fibroblasts
Hyaluronan (HA) is an important constituent of the extracellular matrix and accumulates during inflammatory lung diseases like asthma. Little is known about the factors that regulate HA synthesis by lung cells. Accordingly, we investigated the effect of T-helper 1 (TH1) and 2 (TH2) cytokines and the...
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| Veröffentlicht in: | American journal of respiratory cell and molecular biology 2004-07, Vol.31 (1), p.92-99 |
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| creator | Wilkinson, Thomas S Potter-Perigo, Susan Tsoi, Christina Altman, Leonard C Wight, Thomas N |
| description | Hyaluronan (HA) is an important constituent of the extracellular matrix and accumulates during inflammatory lung diseases like asthma. Little is known about the factors that regulate HA synthesis by lung cells. Accordingly, we investigated the effect of T-helper 1 (TH1) and 2 (TH2) cytokines and the anti-inflammatory agents fluticasone and salmeterol on HA synthesis in human lung fibroblasts. Interleukin-1beta (IL-1beta) and tumor necrosis factor (TNF)-alpha were the most potent stimulators of HA synthesis and when combined, caused synergistic increases in HA accumulation. Time-course analysis of HA accumulation and [3H]-glucosamine incorporation into HA demonstrated continued synthesis over the 24 h of stimulation. Peak synthesis at 6-12 h coincided with an increased proportion of high molecular weight HA. Reverse transcriptase polymerase chain reaction (RT-PCR) revealed that IL-1beta and TNF-alpha induced HA synthase-2 messenger RNA (mRNA) 3 h following stimulation and remained elevated throughout the 24-h stimulation period. Fluticasone inhibited IL-1beta and TNF-alpha induced HA synthesis (44.5%) whereas salmeterol had no effect. When combined, fluticasone and salmeterol inhibited HA synthesis to a greater extent (85.2%). Further, fluticasone attenuated IL-1beta and TNF-alpha stimulated hyaluronan synthase-2 messenger RNA (mRNA), and the addition of salmeterol cooperatively enhanced this inhibition. These results indicate that enhanced synthesis of HA by the proinflammatory cytokines IL-1beta and TNF-alpha can be abrogated by specific corticosteroid and beta2 blocker combinations shown to be effective in the treatment of asthma. |
| doi_str_mv | 10.1165/rcmb.2003-0380OC |
| format | Article |
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Little is known about the factors that regulate HA synthesis by lung cells. Accordingly, we investigated the effect of T-helper 1 (TH1) and 2 (TH2) cytokines and the anti-inflammatory agents fluticasone and salmeterol on HA synthesis in human lung fibroblasts. Interleukin-1beta (IL-1beta) and tumor necrosis factor (TNF)-alpha were the most potent stimulators of HA synthesis and when combined, caused synergistic increases in HA accumulation. Time-course analysis of HA accumulation and [3H]-glucosamine incorporation into HA demonstrated continued synthesis over the 24 h of stimulation. Peak synthesis at 6-12 h coincided with an increased proportion of high molecular weight HA. Reverse transcriptase polymerase chain reaction (RT-PCR) revealed that IL-1beta and TNF-alpha induced HA synthase-2 messenger RNA (mRNA) 3 h following stimulation and remained elevated throughout the 24-h stimulation period. Fluticasone inhibited IL-1beta and TNF-alpha induced HA synthesis (44.5%) whereas salmeterol had no effect. When combined, fluticasone and salmeterol inhibited HA synthesis to a greater extent (85.2%). Further, fluticasone attenuated IL-1beta and TNF-alpha stimulated hyaluronan synthase-2 messenger RNA (mRNA), and the addition of salmeterol cooperatively enhanced this inhibition. These results indicate that enhanced synthesis of HA by the proinflammatory cytokines IL-1beta and TNF-alpha can be abrogated by specific corticosteroid and beta2 blocker combinations shown to be effective in the treatment of asthma.</description><identifier>ISSN: 1044-1549</identifier><identifier>EISSN: 1535-4989</identifier><identifier>DOI: 10.1165/rcmb.2003-0380OC</identifier><identifier>PMID: 14764429</identifier><identifier>CODEN: AJRBEL</identifier><language>eng</language><publisher>United States: Am Thoracic Soc</publisher><subject>Albuterol - analogs & derivatives ; Albuterol - pharmacology ; Androstadienes - pharmacology ; Anti-Inflammatory Agents - pharmacology ; Asthma - immunology ; Asthma - metabolism ; Asthma - physiopathology ; Bronchi - immunology ; Bronchi - metabolism ; Bronchi - physiopathology ; Cells, Cultured ; Cytokines - immunology ; Cytokines - pharmacology ; Drug Interactions - physiology ; Fibroblasts - immunology ; Fibroblasts - metabolism ; Fluticasone ; Glucosamine - pharmacology ; Glucuronosyltransferase ; Humans ; Hyaluronan Synthases ; Hyaluronic Acid - biosynthesis ; Inflammation Mediators - immunology ; Inflammation Mediators - metabolism ; Interleukin-1 - immunology ; Interleukin-1 - pharmacology ; Lung - immunology ; Lung - metabolism ; Pneumonia - immunology ; Pneumonia - metabolism ; Pneumonia - physiopathology ; RNA, Messenger - drug effects ; RNA, Messenger - metabolism ; Salmeterol Xinafoate ; Th1 Cells - immunology ; Th1 Cells - secretion ; Th2 Cells - immunology ; Th2 Cells - secretion ; Transferases - genetics ; Tumor Necrosis Factor-alpha - immunology ; Tumor Necrosis Factor-alpha - pharmacology</subject><ispartof>American journal of respiratory cell and molecular biology, 2004-07, Vol.31 (1), p.92-99</ispartof><rights>Copyright American Thoracic Society Jul 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c462t-699ebb07c2485c49f4d6263c1199711a8b9fad3acfc06fa672976eca79e0a6923</citedby><cites>FETCH-LOGICAL-c462t-699ebb07c2485c49f4d6263c1199711a8b9fad3acfc06fa672976eca79e0a6923</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27907,27908</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14764429$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wilkinson, Thomas S</creatorcontrib><creatorcontrib>Potter-Perigo, Susan</creatorcontrib><creatorcontrib>Tsoi, Christina</creatorcontrib><creatorcontrib>Altman, Leonard C</creatorcontrib><creatorcontrib>Wight, Thomas N</creatorcontrib><title>Pro- and Anti-Inflammatory Factors Cooperate to Control Hyaluronan Synthesis in Lung Fibroblasts</title><title>American journal of respiratory cell and molecular biology</title><addtitle>Am J Respir Cell Mol Biol</addtitle><description>Hyaluronan (HA) is an important constituent of the extracellular matrix and accumulates during inflammatory lung diseases like asthma. Little is known about the factors that regulate HA synthesis by lung cells. Accordingly, we investigated the effect of T-helper 1 (TH1) and 2 (TH2) cytokines and the anti-inflammatory agents fluticasone and salmeterol on HA synthesis in human lung fibroblasts. Interleukin-1beta (IL-1beta) and tumor necrosis factor (TNF)-alpha were the most potent stimulators of HA synthesis and when combined, caused synergistic increases in HA accumulation. Time-course analysis of HA accumulation and [3H]-glucosamine incorporation into HA demonstrated continued synthesis over the 24 h of stimulation. Peak synthesis at 6-12 h coincided with an increased proportion of high molecular weight HA. Reverse transcriptase polymerase chain reaction (RT-PCR) revealed that IL-1beta and TNF-alpha induced HA synthase-2 messenger RNA (mRNA) 3 h following stimulation and remained elevated throughout the 24-h stimulation period. Fluticasone inhibited IL-1beta and TNF-alpha induced HA synthesis (44.5%) whereas salmeterol had no effect. When combined, fluticasone and salmeterol inhibited HA synthesis to a greater extent (85.2%). Further, fluticasone attenuated IL-1beta and TNF-alpha stimulated hyaluronan synthase-2 messenger RNA (mRNA), and the addition of salmeterol cooperatively enhanced this inhibition. These results indicate that enhanced synthesis of HA by the proinflammatory cytokines IL-1beta and TNF-alpha can be abrogated by specific corticosteroid and beta2 blocker combinations shown to be effective in the treatment of asthma.</description><subject>Albuterol - analogs & derivatives</subject><subject>Albuterol - pharmacology</subject><subject>Androstadienes - pharmacology</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Asthma - immunology</subject><subject>Asthma - metabolism</subject><subject>Asthma - physiopathology</subject><subject>Bronchi - immunology</subject><subject>Bronchi - metabolism</subject><subject>Bronchi - physiopathology</subject><subject>Cells, Cultured</subject><subject>Cytokines - immunology</subject><subject>Cytokines - pharmacology</subject><subject>Drug Interactions - physiology</subject><subject>Fibroblasts - immunology</subject><subject>Fibroblasts - metabolism</subject><subject>Fluticasone</subject><subject>Glucosamine - pharmacology</subject><subject>Glucuronosyltransferase</subject><subject>Humans</subject><subject>Hyaluronan Synthases</subject><subject>Hyaluronic Acid - biosynthesis</subject><subject>Inflammation Mediators - immunology</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interleukin-1 - immunology</subject><subject>Interleukin-1 - pharmacology</subject><subject>Lung - immunology</subject><subject>Lung - metabolism</subject><subject>Pneumonia - immunology</subject><subject>Pneumonia - metabolism</subject><subject>Pneumonia - physiopathology</subject><subject>RNA, Messenger - drug effects</subject><subject>RNA, Messenger - metabolism</subject><subject>Salmeterol Xinafoate</subject><subject>Th1 Cells - immunology</subject><subject>Th1 Cells - secretion</subject><subject>Th2 Cells - immunology</subject><subject>Th2 Cells - secretion</subject><subject>Transferases - genetics</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>1044-1549</issn><issn>1535-4989</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpFkE1r4zAQhkXpsunH3nsqopc9udXIsmwdS2jaQqCF3T2rY0VOHGwplWRK_v0qJNDTaOCZd0YPITfA7gFk9RDM2N5zxsqClQ17m5-RC6jKqhCqUef5zYQooBJqRi5j3DIGvAH4SWYgaikEVxfk4z34gqJb0UeX-uLVdQOOIyYf9nSBJtdI597vbMBkafK5cSn4gb7scZiCd-jon71LGxv7SHtHl5Nb00XfBt8OGFO8Jj86HKL9dapX5N_i6e_8pVi-Pb_OH5eFEZKnQipl25bVhoumMkJ1YiW5LA2AUjUANq3qcFWi6QyTHcqaq1pag7WyDKXi5RW5O-bugv-cbEx666fg8krNWf5tXdaQIXaETPAxBtvpXehHDHsNTB-M6oNRfTCqj0bzyO0pd2pHu_oeOCnMwO8jsOnXm68-WB1HHIaMg8btIa8EDTqf-B_OXYCL</recordid><startdate>20040701</startdate><enddate>20040701</enddate><creator>Wilkinson, Thomas S</creator><creator>Potter-Perigo, Susan</creator><creator>Tsoi, Christina</creator><creator>Altman, Leonard C</creator><creator>Wight, Thomas N</creator><general>Am Thoracic Soc</general><general>American Thoracic Society</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope></search><sort><creationdate>20040701</creationdate><title>Pro- and Anti-Inflammatory Factors Cooperate to Control Hyaluronan Synthesis in Lung Fibroblasts</title><author>Wilkinson, Thomas S ; Potter-Perigo, Susan ; Tsoi, Christina ; Altman, Leonard C ; Wight, Thomas N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c462t-699ebb07c2485c49f4d6263c1199711a8b9fad3acfc06fa672976eca79e0a6923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Albuterol - analogs & derivatives</topic><topic>Albuterol - pharmacology</topic><topic>Androstadienes - pharmacology</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Asthma - immunology</topic><topic>Asthma - metabolism</topic><topic>Asthma - physiopathology</topic><topic>Bronchi - immunology</topic><topic>Bronchi - metabolism</topic><topic>Bronchi - physiopathology</topic><topic>Cells, Cultured</topic><topic>Cytokines - immunology</topic><topic>Cytokines - pharmacology</topic><topic>Drug Interactions - physiology</topic><topic>Fibroblasts - immunology</topic><topic>Fibroblasts - metabolism</topic><topic>Fluticasone</topic><topic>Glucosamine - pharmacology</topic><topic>Glucuronosyltransferase</topic><topic>Humans</topic><topic>Hyaluronan Synthases</topic><topic>Hyaluronic Acid - biosynthesis</topic><topic>Inflammation Mediators - immunology</topic><topic>Inflammation Mediators - metabolism</topic><topic>Interleukin-1 - immunology</topic><topic>Interleukin-1 - pharmacology</topic><topic>Lung - immunology</topic><topic>Lung - metabolism</topic><topic>Pneumonia - immunology</topic><topic>Pneumonia - metabolism</topic><topic>Pneumonia - physiopathology</topic><topic>RNA, Messenger - drug effects</topic><topic>RNA, Messenger - metabolism</topic><topic>Salmeterol Xinafoate</topic><topic>Th1 Cells - immunology</topic><topic>Th1 Cells - secretion</topic><topic>Th2 Cells - immunology</topic><topic>Th2 Cells - secretion</topic><topic>Transferases - genetics</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wilkinson, Thomas S</creatorcontrib><creatorcontrib>Potter-Perigo, Susan</creatorcontrib><creatorcontrib>Tsoi, Christina</creatorcontrib><creatorcontrib>Altman, Leonard C</creatorcontrib><creatorcontrib>Wight, Thomas N</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 Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database (ProQuest)</collection><collection>Biological Science Database</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><jtitle>American journal of respiratory cell and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wilkinson, Thomas S</au><au>Potter-Perigo, Susan</au><au>Tsoi, Christina</au><au>Altman, Leonard C</au><au>Wight, Thomas N</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pro- and Anti-Inflammatory Factors Cooperate to Control Hyaluronan Synthesis in Lung Fibroblasts</atitle><jtitle>American journal of respiratory cell and molecular biology</jtitle><addtitle>Am J Respir Cell Mol Biol</addtitle><date>2004-07-01</date><risdate>2004</risdate><volume>31</volume><issue>1</issue><spage>92</spage><epage>99</epage><pages>92-99</pages><issn>1044-1549</issn><eissn>1535-4989</eissn><coden>AJRBEL</coden><abstract>Hyaluronan (HA) is an important constituent of the extracellular matrix and accumulates during inflammatory lung diseases like asthma. Little is known about the factors that regulate HA synthesis by lung cells. Accordingly, we investigated the effect of T-helper 1 (TH1) and 2 (TH2) cytokines and the anti-inflammatory agents fluticasone and salmeterol on HA synthesis in human lung fibroblasts. Interleukin-1beta (IL-1beta) and tumor necrosis factor (TNF)-alpha were the most potent stimulators of HA synthesis and when combined, caused synergistic increases in HA accumulation. Time-course analysis of HA accumulation and [3H]-glucosamine incorporation into HA demonstrated continued synthesis over the 24 h of stimulation. Peak synthesis at 6-12 h coincided with an increased proportion of high molecular weight HA. Reverse transcriptase polymerase chain reaction (RT-PCR) revealed that IL-1beta and TNF-alpha induced HA synthase-2 messenger RNA (mRNA) 3 h following stimulation and remained elevated throughout the 24-h stimulation period. Fluticasone inhibited IL-1beta and TNF-alpha induced HA synthesis (44.5%) whereas salmeterol had no effect. When combined, fluticasone and salmeterol inhibited HA synthesis to a greater extent (85.2%). Further, fluticasone attenuated IL-1beta and TNF-alpha stimulated hyaluronan synthase-2 messenger RNA (mRNA), and the addition of salmeterol cooperatively enhanced this inhibition. These results indicate that enhanced synthesis of HA by the proinflammatory cytokines IL-1beta and TNF-alpha can be abrogated by specific corticosteroid and beta2 blocker combinations shown to be effective in the treatment of asthma.</abstract><cop>United States</cop><pub>Am Thoracic Soc</pub><pmid>14764429</pmid><doi>10.1165/rcmb.2003-0380OC</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete; Alma/SFX Local Collection |
| subjects | Albuterol - analogs & derivatives Albuterol - pharmacology Androstadienes - pharmacology Anti-Inflammatory Agents - pharmacology Asthma - immunology Asthma - metabolism Asthma - physiopathology Bronchi - immunology Bronchi - metabolism Bronchi - physiopathology Cells, Cultured Cytokines - immunology Cytokines - pharmacology Drug Interactions - physiology Fibroblasts - immunology Fibroblasts - metabolism Fluticasone Glucosamine - pharmacology Glucuronosyltransferase Humans Hyaluronan Synthases Hyaluronic Acid - biosynthesis Inflammation Mediators - immunology Inflammation Mediators - metabolism Interleukin-1 - immunology Interleukin-1 - pharmacology Lung - immunology Lung - metabolism Pneumonia - immunology Pneumonia - metabolism Pneumonia - physiopathology RNA, Messenger - drug effects RNA, Messenger - metabolism Salmeterol Xinafoate Th1 Cells - immunology Th1 Cells - secretion Th2 Cells - immunology Th2 Cells - secretion Transferases - genetics Tumor Necrosis Factor-alpha - immunology Tumor Necrosis Factor-alpha - pharmacology |
| title | Pro- and Anti-Inflammatory Factors Cooperate to Control Hyaluronan Synthesis in Lung Fibroblasts |
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