Potential Action of IL-4 and IL-13 as Fibrogenic Factors on Lung Fibroblasts in vitro
Background: Asthma is characterized by chronic inflammation of the airway with the presence of Th2 cytokines. Airway remodeling in asthma is closely related to clinical manifestations. Lung myofibroblasts play a critical role in the airway remodeling and Th2 cytokines may modulate their behavior. We...
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| Veröffentlicht in: | International archives of allergy and immunology 2003-10, Vol.132 (2), p.168-176 |
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| creator | Saito, Akira Okazaki, Hitoshi Sugawara, Isamu Yamamoto, Kazuhiko Takizawa, Hajime |
| description | Background: Asthma is characterized by chronic inflammation of the airway with the presence of Th2 cytokines. Airway remodeling in asthma is closely related to clinical manifestations. Lung myofibroblasts play a critical role in the airway remodeling and Th2 cytokines may modulate their behavior. We examined the effect of two major Th2 cytokines, IL-4 and IL-13, on differentiation of lung fibroblasts to myofibroblasts. We hypothesized that these cytokines would stimulate fibroblast proliferation in association with decreased prostaglandin E 2 (PGE 2 ). Methods: Lung fibroblasts were incubated with IL-4 and IL-13 with or without Th1 cytokine interferon-γ (IFN-γ) in vitro. Differentiation of lung fibroblasts to myofibroblasts was characterized by the expression of α-smooth muscle actin (α-SMA) as well as a morphological and immunohistochemical analysis. Fibroblast proliferation stimulated by IL-4 and IL-13 was assessed with the MTT assay. We also investigated the effect of these cytokines on cyclooxygenase (COX) gene expression and PGE 2 production. Results: IL-4 and IL-13 increased α-SMA expression and myofibroblastic differentiation. This effect was attenuated by IFN-γ and dexamethasone failed to have an influence on differentiation. IL-4 and IL-13 stimulated fibroblast proliferation. These cytokines downregulated the expression of both COX-1 and COX-2 genes and decreased the production of PGE 2 . Conclusions: IL-4 and IL-13 induce differentiation of fibroblasts to myofibroblasts and this response is attenuated by IFN-γ. IL-4 and IL-13 stimulate fibroblast proliferation and this effect is at least partly due to suppressed COX gene expressions and subsequently decreased PGE 2 production. These findings suggest that IL-4 and IL-13 directly act on lung fibroblast to induce a fibrogenic response. |
| doi_str_mv | 10.1159/000073718 |
| format | Article |
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Airway remodeling in asthma is closely related to clinical manifestations. Lung myofibroblasts play a critical role in the airway remodeling and Th2 cytokines may modulate their behavior. We examined the effect of two major Th2 cytokines, IL-4 and IL-13, on differentiation of lung fibroblasts to myofibroblasts. We hypothesized that these cytokines would stimulate fibroblast proliferation in association with decreased prostaglandin E 2 (PGE 2 ). Methods: Lung fibroblasts were incubated with IL-4 and IL-13 with or without Th1 cytokine interferon-γ (IFN-γ) in vitro. Differentiation of lung fibroblasts to myofibroblasts was characterized by the expression of α-smooth muscle actin (α-SMA) as well as a morphological and immunohistochemical analysis. Fibroblast proliferation stimulated by IL-4 and IL-13 was assessed with the MTT assay. We also investigated the effect of these cytokines on cyclooxygenase (COX) gene expression and PGE 2 production. Results: IL-4 and IL-13 increased α-SMA expression and myofibroblastic differentiation. This effect was attenuated by IFN-γ and dexamethasone failed to have an influence on differentiation. IL-4 and IL-13 stimulated fibroblast proliferation. These cytokines downregulated the expression of both COX-1 and COX-2 genes and decreased the production of PGE 2 . Conclusions: IL-4 and IL-13 induce differentiation of fibroblasts to myofibroblasts and this response is attenuated by IFN-γ. IL-4 and IL-13 stimulate fibroblast proliferation and this effect is at least partly due to suppressed COX gene expressions and subsequently decreased PGE 2 production. These findings suggest that IL-4 and IL-13 directly act on lung fibroblast to induce a fibrogenic response.</description><identifier>ISSN: 1018-2438</identifier><identifier>EISSN: 1423-0097</identifier><identifier>DOI: 10.1159/000073718</identifier><identifier>PMID: 14600429</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Actins - immunology ; Actins - metabolism ; Allergic diseases ; Biological and medical sciences ; Cell Differentiation - immunology ; Cell Division - drug effects ; Cells, Cultured ; Cyclooxygenase 1 ; Cyclooxygenase 2 ; Dinoprostone - antagonists & inhibitors ; Dinoprostone - metabolism ; Dinoprostone - secretion ; Fibroblasts - cytology ; Fibroblasts - drug effects ; Fibroblasts - immunology ; Fibroblasts - metabolism ; Fibrosis - immunology ; Humans ; Immunohistochemistry ; Immunopathology ; Indomethacin - pharmacology ; Interferon-gamma - immunology ; Interferon-gamma - pharmacology ; Interleukin-13 - immunology ; Interleukin-13 - pharmacology ; Interleukin-4 - genetics ; Interleukin-4 - immunology ; Interleukin-4 - pharmacology ; Isoenzymes - biosynthesis ; Isoenzymes - genetics ; Lung - cytology ; Lung - drug effects ; Lung - immunology ; Lung - metabolism ; Medical sciences ; Membrane Proteins ; Original Paper ; Prostaglandin-Endoperoxide Synthases - biosynthesis ; Prostaglandin-Endoperoxide Synthases - genetics ; Respiratory and ent allergic diseases ; Reverse Transcriptase Polymerase Chain Reaction ; RNA - chemistry ; RNA - genetics ; Transforming Growth Factor beta - pharmacology ; Transforming Growth Factor beta1</subject><ispartof>International archives of allergy and immunology, 2003-10, Vol.132 (2), p.168-176</ispartof><rights>2003 S. Karger AG, Basel</rights><rights>Copyright 2003 S. Karger AG, Basel</rights><rights>Copyright (c) 2003 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-dd86d422555c516ecfdf6e62c85aa284854667c1bd8492386aa78637ef3d11613</citedby><cites>FETCH-LOGICAL-c455t-dd86d422555c516ecfdf6e62c85aa284854667c1bd8492386aa78637ef3d11613</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2423,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15439900$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14600429$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Saito, Akira</creatorcontrib><creatorcontrib>Okazaki, Hitoshi</creatorcontrib><creatorcontrib>Sugawara, Isamu</creatorcontrib><creatorcontrib>Yamamoto, Kazuhiko</creatorcontrib><creatorcontrib>Takizawa, Hajime</creatorcontrib><title>Potential Action of IL-4 and IL-13 as Fibrogenic Factors on Lung Fibroblasts in vitro</title><title>International archives of allergy and immunology</title><addtitle>Int Arch Allergy Immunol</addtitle><description>Background: Asthma is characterized by chronic inflammation of the airway with the presence of Th2 cytokines. Airway remodeling in asthma is closely related to clinical manifestations. Lung myofibroblasts play a critical role in the airway remodeling and Th2 cytokines may modulate their behavior. We examined the effect of two major Th2 cytokines, IL-4 and IL-13, on differentiation of lung fibroblasts to myofibroblasts. We hypothesized that these cytokines would stimulate fibroblast proliferation in association with decreased prostaglandin E 2 (PGE 2 ). Methods: Lung fibroblasts were incubated with IL-4 and IL-13 with or without Th1 cytokine interferon-γ (IFN-γ) in vitro. Differentiation of lung fibroblasts to myofibroblasts was characterized by the expression of α-smooth muscle actin (α-SMA) as well as a morphological and immunohistochemical analysis. Fibroblast proliferation stimulated by IL-4 and IL-13 was assessed with the MTT assay. We also investigated the effect of these cytokines on cyclooxygenase (COX) gene expression and PGE 2 production. Results: IL-4 and IL-13 increased α-SMA expression and myofibroblastic differentiation. This effect was attenuated by IFN-γ and dexamethasone failed to have an influence on differentiation. IL-4 and IL-13 stimulated fibroblast proliferation. These cytokines downregulated the expression of both COX-1 and COX-2 genes and decreased the production of PGE 2 . Conclusions: IL-4 and IL-13 induce differentiation of fibroblasts to myofibroblasts and this response is attenuated by IFN-γ. IL-4 and IL-13 stimulate fibroblast proliferation and this effect is at least partly due to suppressed COX gene expressions and subsequently decreased PGE 2 production. These findings suggest that IL-4 and IL-13 directly act on lung fibroblast to induce a fibrogenic response.</description><subject>Actins - immunology</subject><subject>Actins - metabolism</subject><subject>Allergic diseases</subject><subject>Biological and medical sciences</subject><subject>Cell Differentiation - immunology</subject><subject>Cell Division - drug effects</subject><subject>Cells, Cultured</subject><subject>Cyclooxygenase 1</subject><subject>Cyclooxygenase 2</subject><subject>Dinoprostone - antagonists & inhibitors</subject><subject>Dinoprostone - metabolism</subject><subject>Dinoprostone - secretion</subject><subject>Fibroblasts - cytology</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - immunology</subject><subject>Fibroblasts - metabolism</subject><subject>Fibrosis - immunology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Immunopathology</subject><subject>Indomethacin - pharmacology</subject><subject>Interferon-gamma - immunology</subject><subject>Interferon-gamma - pharmacology</subject><subject>Interleukin-13 - immunology</subject><subject>Interleukin-13 - pharmacology</subject><subject>Interleukin-4 - genetics</subject><subject>Interleukin-4 - immunology</subject><subject>Interleukin-4 - pharmacology</subject><subject>Isoenzymes - biosynthesis</subject><subject>Isoenzymes - genetics</subject><subject>Lung - cytology</subject><subject>Lung - drug effects</subject><subject>Lung - immunology</subject><subject>Lung - metabolism</subject><subject>Medical sciences</subject><subject>Membrane Proteins</subject><subject>Original Paper</subject><subject>Prostaglandin-Endoperoxide Synthases - biosynthesis</subject><subject>Prostaglandin-Endoperoxide Synthases - genetics</subject><subject>Respiratory and ent allergic diseases</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA - chemistry</subject><subject>RNA - genetics</subject><subject>Transforming Growth Factor beta - pharmacology</subject><subject>Transforming Growth Factor beta1</subject><issn>1018-2438</issn><issn>1423-0097</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqF0c1LHDEYBvAgLfWjPXguSBAUehibN985irgqLLQHPQ_ZTGaJnU1sMiP435tlFgUv5pIX8uMJLw9Cx0AuAIT5TepRTIHeQwfAKWsIMepLnQnohnKm99FhKY-EVKzlN7QPXBLCqTlAD3_T6OMY7IAv3RhSxKnHd8uGYxu77QAM24IXYZXT2sfg8MK6MeWCK11OcT0_rQZbxoJDxM9hzOk7-trbofgfu_sIPSyu769um-Wfm7ury2XjuBBj03VadpxSIYQTIL3ru156SZ0W1lLNteBSKgerTnNDmZbWKi2Z8j3rACSwI3Q-5z7l9H_yZWw3oTg_DDb6NJVWAeNcK_UpBEMpB6ErPP0AH9OUY12ipRS0oMZs037NyOVUSvZ9-5TDxuaXFki7baR9a6Tak13gtNr47l3uKqjgbAdscXbos40ulHcnODOGkOp-zu6fzWuf38D8zSufkpdP</recordid><startdate>20031001</startdate><enddate>20031001</enddate><creator>Saito, Akira</creator><creator>Okazaki, Hitoshi</creator><creator>Sugawara, Isamu</creator><creator>Yamamoto, Kazuhiko</creator><creator>Takizawa, Hajime</creator><general>Karger</general><general>S. 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immunology</topic><topic>Actins - metabolism</topic><topic>Allergic diseases</topic><topic>Biological and medical sciences</topic><topic>Cell Differentiation - immunology</topic><topic>Cell Division - drug effects</topic><topic>Cells, Cultured</topic><topic>Cyclooxygenase 1</topic><topic>Cyclooxygenase 2</topic><topic>Dinoprostone - antagonists & inhibitors</topic><topic>Dinoprostone - metabolism</topic><topic>Dinoprostone - secretion</topic><topic>Fibroblasts - cytology</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - immunology</topic><topic>Fibroblasts - metabolism</topic><topic>Fibrosis - immunology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Immunopathology</topic><topic>Indomethacin - pharmacology</topic><topic>Interferon-gamma - immunology</topic><topic>Interferon-gamma - pharmacology</topic><topic>Interleukin-13 - immunology</topic><topic>Interleukin-13 - pharmacology</topic><topic>Interleukin-4 - genetics</topic><topic>Interleukin-4 - 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Academic</collection><jtitle>International archives of allergy and immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Saito, Akira</au><au>Okazaki, Hitoshi</au><au>Sugawara, Isamu</au><au>Yamamoto, Kazuhiko</au><au>Takizawa, Hajime</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Potential Action of IL-4 and IL-13 as Fibrogenic Factors on Lung Fibroblasts in vitro</atitle><jtitle>International archives of allergy and immunology</jtitle><addtitle>Int Arch Allergy Immunol</addtitle><date>2003-10-01</date><risdate>2003</risdate><volume>132</volume><issue>2</issue><spage>168</spage><epage>176</epage><pages>168-176</pages><issn>1018-2438</issn><eissn>1423-0097</eissn><abstract>Background: Asthma is characterized by chronic inflammation of the airway with the presence of Th2 cytokines. Airway remodeling in asthma is closely related to clinical manifestations. Lung myofibroblasts play a critical role in the airway remodeling and Th2 cytokines may modulate their behavior. We examined the effect of two major Th2 cytokines, IL-4 and IL-13, on differentiation of lung fibroblasts to myofibroblasts. We hypothesized that these cytokines would stimulate fibroblast proliferation in association with decreased prostaglandin E 2 (PGE 2 ). Methods: Lung fibroblasts were incubated with IL-4 and IL-13 with or without Th1 cytokine interferon-γ (IFN-γ) in vitro. Differentiation of lung fibroblasts to myofibroblasts was characterized by the expression of α-smooth muscle actin (α-SMA) as well as a morphological and immunohistochemical analysis. Fibroblast proliferation stimulated by IL-4 and IL-13 was assessed with the MTT assay. We also investigated the effect of these cytokines on cyclooxygenase (COX) gene expression and PGE 2 production. Results: IL-4 and IL-13 increased α-SMA expression and myofibroblastic differentiation. This effect was attenuated by IFN-γ and dexamethasone failed to have an influence on differentiation. IL-4 and IL-13 stimulated fibroblast proliferation. These cytokines downregulated the expression of both COX-1 and COX-2 genes and decreased the production of PGE 2 . Conclusions: IL-4 and IL-13 induce differentiation of fibroblasts to myofibroblasts and this response is attenuated by IFN-γ. IL-4 and IL-13 stimulate fibroblast proliferation and this effect is at least partly due to suppressed COX gene expressions and subsequently decreased PGE 2 production. These findings suggest that IL-4 and IL-13 directly act on lung fibroblast to induce a fibrogenic response.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>14600429</pmid><doi>10.1159/000073718</doi><tpages>9</tpages></addata></record> |
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| subjects | Actins - immunology Actins - metabolism Allergic diseases Biological and medical sciences Cell Differentiation - immunology Cell Division - drug effects Cells, Cultured Cyclooxygenase 1 Cyclooxygenase 2 Dinoprostone - antagonists & inhibitors Dinoprostone - metabolism Dinoprostone - secretion Fibroblasts - cytology Fibroblasts - drug effects Fibroblasts - immunology Fibroblasts - metabolism Fibrosis - immunology Humans Immunohistochemistry Immunopathology Indomethacin - pharmacology Interferon-gamma - immunology Interferon-gamma - pharmacology Interleukin-13 - immunology Interleukin-13 - pharmacology Interleukin-4 - genetics Interleukin-4 - immunology Interleukin-4 - pharmacology Isoenzymes - biosynthesis Isoenzymes - genetics Lung - cytology Lung - drug effects Lung - immunology Lung - metabolism Medical sciences Membrane Proteins Original Paper Prostaglandin-Endoperoxide Synthases - biosynthesis Prostaglandin-Endoperoxide Synthases - genetics Respiratory and ent allergic diseases Reverse Transcriptase Polymerase Chain Reaction RNA - chemistry RNA - genetics Transforming Growth Factor beta - pharmacology Transforming Growth Factor beta1 |
| title | Potential Action of IL-4 and IL-13 as Fibrogenic Factors on Lung Fibroblasts in vitro |
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