Role of thrombin in interleukin-5 expression from basophils
Interleukin-5 (IL-5) plays a key role in the pathogenesis of bronchial asthma. Thrombin is a procoagulant factor that has been also reported to participate in the inflammatory response by stimulating the secretion of cytokines. Interaction of inflammatory cells with airway epithelial cells may also...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2008-03, Vol.368 (1), p.116-120 |
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| creator | Yamaguchi, Aiko Gabazza, Esteban C. Takei, Yoshiyuki Yano, Yutaka Fujimoto, Hajime D’Alessandro-Gabazza, Corina N. Murakami, Eiko Kobayashi, Tetsu Takagi, Takehiro Maruyama, Junko Suzuki, Koji Taguchi, Osamu |
| description | Interleukin-5 (IL-5) plays a key role in the pathogenesis of bronchial asthma. Thrombin is a procoagulant factor that has been also reported to participate in the inflammatory response by stimulating the secretion of cytokines. Interaction of inflammatory cells with airway epithelial cells may also promote the secretion of cytokines. However, the role of thrombin and cell-to-cell interaction in pathogenesis of allergic inflammation is unclear. In this study, we evaluated the role of thrombin and cell-to-cell interaction in the secretion of IL-5 from basophils. The human basophil cell line KU-812 was used in the assays. Thrombin and co-culture with alveolar epithelial cells significantly stimulated the secretion of IL-5 from KU-812 cells as compared to controls. Secretion of IL-5 was synergistically stimulated when KU-812 cells were incubated in the presence of both thrombin and alveolar epithelial cells. Co-culture of KU-812 cells with epithelial cells significantly increased the expression of tissue factor, an activator of coagulation activation, in a cell dose-dependent manner. Secretion of IL-5 from KU-812 basophils co-cultured with epithelial cells was significantly inhibited by LY294002, an inhibitor of phosphatidylinositol 3-kinase. These results suggest that thrombin and cell interaction with lung epithelial cells may augment the inflammatory response in allergic diseases by stimulating the secretion of IL-5 from basophils. |
| doi_str_mv | 10.1016/j.bbrc.2008.01.048 |
| format | Article |
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Thrombin is a procoagulant factor that has been also reported to participate in the inflammatory response by stimulating the secretion of cytokines. Interaction of inflammatory cells with airway epithelial cells may also promote the secretion of cytokines. However, the role of thrombin and cell-to-cell interaction in pathogenesis of allergic inflammation is unclear. In this study, we evaluated the role of thrombin and cell-to-cell interaction in the secretion of IL-5 from basophils. The human basophil cell line KU-812 was used in the assays. Thrombin and co-culture with alveolar epithelial cells significantly stimulated the secretion of IL-5 from KU-812 cells as compared to controls. Secretion of IL-5 was synergistically stimulated when KU-812 cells were incubated in the presence of both thrombin and alveolar epithelial cells. Co-culture of KU-812 cells with epithelial cells significantly increased the expression of tissue factor, an activator of coagulation activation, in a cell dose-dependent manner. Secretion of IL-5 from KU-812 basophils co-cultured with epithelial cells was significantly inhibited by LY294002, an inhibitor of phosphatidylinositol 3-kinase. These results suggest that thrombin and cell interaction with lung epithelial cells may augment the inflammatory response in allergic diseases by stimulating the secretion of IL-5 from basophils.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2008.01.048</identifier><identifier>PMID: 18206982</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Allergy ; Basophils - drug effects ; Basophils - metabolism ; Basophils - secretion ; Bronchial asthma ; Cell Line ; Coagulation ; Coculture Techniques ; Epithelial Cells - drug effects ; Epithelial Cells - secretion ; Humans ; Interleukin-5 ; Interleukin-5 - metabolism ; Interleukin-5 - secretion ; Phosphatidylinositol 3-Kinases - antagonists & inhibitors ; Phosphatidylinositol 3-Kinases - metabolism ; Protein Kinase Inhibitors - pharmacology ; Receptors, Thrombin - metabolism ; Thrombin ; Thrombin - pharmacology</subject><ispartof>Biochemical and biophysical research communications, 2008-03, Vol.368 (1), p.116-120</ispartof><rights>2008 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-905d75517821d88ef0af42237e4cbf2d6691f6ed6c54dd3c1193e3ec6e48adf33</citedby><cites>FETCH-LOGICAL-c451t-905d75517821d88ef0af42237e4cbf2d6691f6ed6c54dd3c1193e3ec6e48adf33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X08000879$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18206982$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yamaguchi, Aiko</creatorcontrib><creatorcontrib>Gabazza, Esteban C.</creatorcontrib><creatorcontrib>Takei, Yoshiyuki</creatorcontrib><creatorcontrib>Yano, Yutaka</creatorcontrib><creatorcontrib>Fujimoto, Hajime</creatorcontrib><creatorcontrib>D’Alessandro-Gabazza, Corina N.</creatorcontrib><creatorcontrib>Murakami, Eiko</creatorcontrib><creatorcontrib>Kobayashi, Tetsu</creatorcontrib><creatorcontrib>Takagi, Takehiro</creatorcontrib><creatorcontrib>Maruyama, Junko</creatorcontrib><creatorcontrib>Suzuki, Koji</creatorcontrib><creatorcontrib>Taguchi, Osamu</creatorcontrib><title>Role of thrombin in interleukin-5 expression from basophils</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Interleukin-5 (IL-5) plays a key role in the pathogenesis of bronchial asthma. Thrombin is a procoagulant factor that has been also reported to participate in the inflammatory response by stimulating the secretion of cytokines. Interaction of inflammatory cells with airway epithelial cells may also promote the secretion of cytokines. However, the role of thrombin and cell-to-cell interaction in pathogenesis of allergic inflammation is unclear. In this study, we evaluated the role of thrombin and cell-to-cell interaction in the secretion of IL-5 from basophils. The human basophil cell line KU-812 was used in the assays. Thrombin and co-culture with alveolar epithelial cells significantly stimulated the secretion of IL-5 from KU-812 cells as compared to controls. Secretion of IL-5 was synergistically stimulated when KU-812 cells were incubated in the presence of both thrombin and alveolar epithelial cells. Co-culture of KU-812 cells with epithelial cells significantly increased the expression of tissue factor, an activator of coagulation activation, in a cell dose-dependent manner. Secretion of IL-5 from KU-812 basophils co-cultured with epithelial cells was significantly inhibited by LY294002, an inhibitor of phosphatidylinositol 3-kinase. These results suggest that thrombin and cell interaction with lung epithelial cells may augment the inflammatory response in allergic diseases by stimulating the secretion of IL-5 from basophils.</description><subject>Allergy</subject><subject>Basophils - drug effects</subject><subject>Basophils - metabolism</subject><subject>Basophils - secretion</subject><subject>Bronchial asthma</subject><subject>Cell Line</subject><subject>Coagulation</subject><subject>Coculture Techniques</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - secretion</subject><subject>Humans</subject><subject>Interleukin-5</subject><subject>Interleukin-5 - metabolism</subject><subject>Interleukin-5 - secretion</subject><subject>Phosphatidylinositol 3-Kinases - antagonists & inhibitors</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Receptors, Thrombin - metabolism</subject><subject>Thrombin</subject><subject>Thrombin - pharmacology</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1r3DAURUVISaZJ_kAWxavs7L4n27JEsimhXxAIlAayE7b0RDS1rYnkKe2_j6YzkF0DD-7m3AvvMHaJUCGg-LiuhiGaigPICrCCRh6xFYKCkiM0x2wFAKLkCh9P2fuU1gCIjVAn7BQlB6EkX7HrH2GkIrhieYphGvxc_LuF4kjbX34u24L-bCKl5MNcuMwUQ5_C5smP6Zy9c_2Y6OKQZ-zhy-eft9_Ku_uv328_3ZWmaXEpFbS2a1vsJEcrJTnoXcN53VFjBsetEAqdICtM21hbG0RVU01GUCN76-r6jF3tdzcxPG8pLXryydA49jOFbdIdcCXa3HoLzE9nV6rNIN-DJoaUIjm9iX7q41-NoHdu9Vrv3OqdWw2os9tc-nBY3w4T2dfKQWYGbvYAZRm_PUWdjKfZkPWRzKJt8P_bfwHS6IoG</recordid><startdate>20080328</startdate><enddate>20080328</enddate><creator>Yamaguchi, Aiko</creator><creator>Gabazza, Esteban C.</creator><creator>Takei, Yoshiyuki</creator><creator>Yano, Yutaka</creator><creator>Fujimoto, Hajime</creator><creator>D’Alessandro-Gabazza, Corina N.</creator><creator>Murakami, Eiko</creator><creator>Kobayashi, Tetsu</creator><creator>Takagi, Takehiro</creator><creator>Maruyama, Junko</creator><creator>Suzuki, Koji</creator><creator>Taguchi, Osamu</creator><general>Elsevier 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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20080328</creationdate><title>Role of thrombin in interleukin-5 expression from basophils</title><author>Yamaguchi, Aiko ; Gabazza, Esteban C. ; Takei, Yoshiyuki ; Yano, Yutaka ; Fujimoto, Hajime ; D’Alessandro-Gabazza, Corina N. ; Murakami, Eiko ; Kobayashi, Tetsu ; Takagi, Takehiro ; Maruyama, Junko ; Suzuki, Koji ; Taguchi, Osamu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-905d75517821d88ef0af42237e4cbf2d6691f6ed6c54dd3c1193e3ec6e48adf33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Allergy</topic><topic>Basophils - drug effects</topic><topic>Basophils - metabolism</topic><topic>Basophils - secretion</topic><topic>Bronchial asthma</topic><topic>Cell Line</topic><topic>Coagulation</topic><topic>Coculture Techniques</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - secretion</topic><topic>Humans</topic><topic>Interleukin-5</topic><topic>Interleukin-5 - metabolism</topic><topic>Interleukin-5 - secretion</topic><topic>Phosphatidylinositol 3-Kinases - antagonists & inhibitors</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Receptors, Thrombin - metabolism</topic><topic>Thrombin</topic><topic>Thrombin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yamaguchi, Aiko</creatorcontrib><creatorcontrib>Gabazza, Esteban C.</creatorcontrib><creatorcontrib>Takei, Yoshiyuki</creatorcontrib><creatorcontrib>Yano, Yutaka</creatorcontrib><creatorcontrib>Fujimoto, Hajime</creatorcontrib><creatorcontrib>D’Alessandro-Gabazza, Corina N.</creatorcontrib><creatorcontrib>Murakami, Eiko</creatorcontrib><creatorcontrib>Kobayashi, Tetsu</creatorcontrib><creatorcontrib>Takagi, Takehiro</creatorcontrib><creatorcontrib>Maruyama, Junko</creatorcontrib><creatorcontrib>Suzuki, Koji</creatorcontrib><creatorcontrib>Taguchi, Osamu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yamaguchi, Aiko</au><au>Gabazza, Esteban C.</au><au>Takei, Yoshiyuki</au><au>Yano, Yutaka</au><au>Fujimoto, Hajime</au><au>D’Alessandro-Gabazza, Corina N.</au><au>Murakami, Eiko</au><au>Kobayashi, Tetsu</au><au>Takagi, Takehiro</au><au>Maruyama, Junko</au><au>Suzuki, Koji</au><au>Taguchi, Osamu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of thrombin in interleukin-5 expression from basophils</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2008-03-28</date><risdate>2008</risdate><volume>368</volume><issue>1</issue><spage>116</spage><epage>120</epage><pages>116-120</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Interleukin-5 (IL-5) plays a key role in the pathogenesis of bronchial asthma. Thrombin is a procoagulant factor that has been also reported to participate in the inflammatory response by stimulating the secretion of cytokines. Interaction of inflammatory cells with airway epithelial cells may also promote the secretion of cytokines. However, the role of thrombin and cell-to-cell interaction in pathogenesis of allergic inflammation is unclear. In this study, we evaluated the role of thrombin and cell-to-cell interaction in the secretion of IL-5 from basophils. The human basophil cell line KU-812 was used in the assays. Thrombin and co-culture with alveolar epithelial cells significantly stimulated the secretion of IL-5 from KU-812 cells as compared to controls. Secretion of IL-5 was synergistically stimulated when KU-812 cells were incubated in the presence of both thrombin and alveolar epithelial cells. Co-culture of KU-812 cells with epithelial cells significantly increased the expression of tissue factor, an activator of coagulation activation, in a cell dose-dependent manner. Secretion of IL-5 from KU-812 basophils co-cultured with epithelial cells was significantly inhibited by LY294002, an inhibitor of phosphatidylinositol 3-kinase. These results suggest that thrombin and cell interaction with lung epithelial cells may augment the inflammatory response in allergic diseases by stimulating the secretion of IL-5 from basophils.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>18206982</pmid><doi>10.1016/j.bbrc.2008.01.048</doi><tpages>5</tpages></addata></record> |
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| ispartof | Biochemical and biophysical research communications, 2008-03, Vol.368 (1), p.116-120 |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Allergy Basophils - drug effects Basophils - metabolism Basophils - secretion Bronchial asthma Cell Line Coagulation Coculture Techniques Epithelial Cells - drug effects Epithelial Cells - secretion Humans Interleukin-5 Interleukin-5 - metabolism Interleukin-5 - secretion Phosphatidylinositol 3-Kinases - antagonists & inhibitors Phosphatidylinositol 3-Kinases - metabolism Protein Kinase Inhibitors - pharmacology Receptors, Thrombin - metabolism Thrombin Thrombin - pharmacology |
| title | Role of thrombin in interleukin-5 expression from basophils |
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