N-acetylcysteine reduces chemokine release via inhibition of p38 MAPK in human airway smooth muscle cells
Reactive oxygen species are involved in the activation of several mitogen-activated protein kinases (MAPKs), key-players in the production of several cytokines. Therefore the current study investigated whether N-acetylcysteine (NAC), an antioxidative agent, inhibits the interleukin (IL)-1beta-induce...
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| Veröffentlicht in: | The European respiratory journal 2003-07, Vol.22 (1), p.43-49 |
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| creator | Wuyts, W.A Vanaudenaerde, B.M Dupont, L.J Demedts, M.G Verleden, G.M |
| description | Reactive oxygen species are involved in the activation of several mitogen-activated protein kinases (MAPKs), key-players in the production of several cytokines. Therefore the current study investigated whether N-acetylcysteine (NAC), an antioxidative agent, inhibits the interleukin (IL)-1beta-induced expression and production of eotaxin and monocyte chemotactic protein (MCP)-1 in human airway smooth muscle cells (HASMC). NAC (10 mM) decreased the expression of eotaxin and MCP-1, by 46 +/- 11% (n=7) and 87 +/- 4% (n=6), respectively; the eotaxin release was inhibited by 75 +/- 5% (n=7), whereas the MCP-1 release was decreased by 69 +/- 41% (n=10). NAC (1 mM) also decreased the IL-1beta-induced activation of p38 MAPK. Compared with unstimulated cells, a four-fold increase in 8-isoprostane production in IL-1beta-stimulated HASMC was observed, which could be inhibited by NAC in a concentration-dependent way, with a maximum inhibition of 39 +/- 12%, with 1 mM NAC. The present study demonstrated that N-acetylcysteine inhibits the interleukin-1beta-induced eotaxin and monocyte chemotactic protein 1 expression and production due to a decreased activation of p38 mitogen-activated protein kinase. This study has also shown that N-acetylcysteine decreases the interleukin-1beta-induced production of reactive oxygen species, as suggested by a reduction in the 8-isoprostane production. |
| doi_str_mv | 10.1183/09031936.03.00064803 |
| format | Article |
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Therefore the current study investigated whether N-acetylcysteine (NAC), an antioxidative agent, inhibits the interleukin (IL)-1beta-induced expression and production of eotaxin and monocyte chemotactic protein (MCP)-1 in human airway smooth muscle cells (HASMC). NAC (10 mM) decreased the expression of eotaxin and MCP-1, by 46 +/- 11% (n=7) and 87 +/- 4% (n=6), respectively; the eotaxin release was inhibited by 75 +/- 5% (n=7), whereas the MCP-1 release was decreased by 69 +/- 41% (n=10). NAC (1 mM) also decreased the IL-1beta-induced activation of p38 MAPK. Compared with unstimulated cells, a four-fold increase in 8-isoprostane production in IL-1beta-stimulated HASMC was observed, which could be inhibited by NAC in a concentration-dependent way, with a maximum inhibition of 39 +/- 12%, with 1 mM NAC. The present study demonstrated that N-acetylcysteine inhibits the interleukin-1beta-induced eotaxin and monocyte chemotactic protein 1 expression and production due to a decreased activation of p38 mitogen-activated protein kinase. This study has also shown that N-acetylcysteine decreases the interleukin-1beta-induced production of reactive oxygen species, as suggested by a reduction in the 8-isoprostane production.</description><identifier>ISSN: 0903-1936</identifier><identifier>EISSN: 1399-3003</identifier><identifier>DOI: 10.1183/09031936.03.00064803</identifier><identifier>PMID: 12882449</identifier><language>eng</language><publisher>Leeds: Eur Respiratory Soc</publisher><subject>Acetylcysteine - pharmacology ; Asthma - enzymology ; Asthma - immunology ; Biological and medical sciences ; Blotting, Northern ; Cells, Cultured ; Chemokine CCL11 ; Chemokine CCL2 - metabolism ; Chemokines - metabolism ; Chemokines, CC - antagonists & inhibitors ; Chemokines, CC - metabolism ; Digestive system ; Dinoprost - analogs & derivatives ; Enzyme Activation ; Enzyme-Linked Immunosorbent Assay ; F2-Isoprostanes - metabolism ; Humans ; Interleukin-1 - pharmacology ; Investigative techniques, diagnostic techniques (general aspects) ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 4 ; MAP Kinase Signaling System ; Medical sciences ; Mitogen-Activated Protein Kinase Kinases ; Mitogen-Activated Protein Kinases - antagonists & inhibitors ; Mitogen-Activated Protein Kinases - metabolism ; Muscle, Smooth - drug effects ; Muscle, Smooth - enzymology ; Muscle, Smooth - immunology ; p38 Mitogen-Activated Protein Kinases ; Pathology. Cytology. Biochemistry. Spectrometry. 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Therefore the current study investigated whether N-acetylcysteine (NAC), an antioxidative agent, inhibits the interleukin (IL)-1beta-induced expression and production of eotaxin and monocyte chemotactic protein (MCP)-1 in human airway smooth muscle cells (HASMC). NAC (10 mM) decreased the expression of eotaxin and MCP-1, by 46 +/- 11% (n=7) and 87 +/- 4% (n=6), respectively; the eotaxin release was inhibited by 75 +/- 5% (n=7), whereas the MCP-1 release was decreased by 69 +/- 41% (n=10). NAC (1 mM) also decreased the IL-1beta-induced activation of p38 MAPK. Compared with unstimulated cells, a four-fold increase in 8-isoprostane production in IL-1beta-stimulated HASMC was observed, which could be inhibited by NAC in a concentration-dependent way, with a maximum inhibition of 39 +/- 12%, with 1 mM NAC. The present study demonstrated that N-acetylcysteine inhibits the interleukin-1beta-induced eotaxin and monocyte chemotactic protein 1 expression and production due to a decreased activation of p38 mitogen-activated protein kinase. This study has also shown that N-acetylcysteine decreases the interleukin-1beta-induced production of reactive oxygen species, as suggested by a reduction in the 8-isoprostane production.</description><subject>Acetylcysteine - pharmacology</subject><subject>Asthma - enzymology</subject><subject>Asthma - immunology</subject><subject>Biological and medical sciences</subject><subject>Blotting, Northern</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL11</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Chemokines - metabolism</subject><subject>Chemokines, CC - antagonists & inhibitors</subject><subject>Chemokines, CC - metabolism</subject><subject>Digestive system</subject><subject>Dinoprost - analogs & derivatives</subject><subject>Enzyme Activation</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>F2-Isoprostanes - metabolism</subject><subject>Humans</subject><subject>Interleukin-1 - pharmacology</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>JNK Mitogen-Activated Protein Kinases</subject><subject>MAP Kinase Kinase 4</subject><subject>MAP Kinase Signaling System</subject><subject>Medical sciences</subject><subject>Mitogen-Activated Protein Kinase Kinases</subject><subject>Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Muscle, Smooth - drug effects</subject><subject>Muscle, Smooth - enzymology</subject><subject>Muscle, Smooth - immunology</subject><subject>p38 Mitogen-Activated Protein Kinases</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>Signal Transduction</subject><subject>Statistics, Nonparametric</subject><subject>Stimulation, Chemical</subject><issn>0903-1936</issn><issn>1399-3003</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMuO1DAQRS0EYpqBP0DIC2CXpsrlJM5yNBoeYngsYG05ToV4yKOxE0b99yTqRrOqUuncq9IR4iXCHtHQO6iAsKJiD7QHgEIboEdih1RVGQHQY7HbkGxjLsSzlO4AsNCET8UFKmOU1tVOhK-Z8zwfe39MM4eRZeRm8Zyk73iYfp8uPbvE8m9wMoxdqMMcplFOrTyQkV-uvn9ez7JbBjdKF-K9O8o0TNPcyWFJvmfpue_Tc_GkdX3iF-d5KX6-v_lx_TG7_fbh0_XVbeapUHPWsC7yssbWecMmd65AIjIIJTaVqbFEo31TKUfQalRcl6C5YGippoaLhi7F21PvIU5_Fk6zHULaPnAjT0uyJeVKYZ6voD6BPk4pRW7tIYbBxaNFsJti-1-xhXU_K15jr879Sz1w8xA6O12BN2fAJe_6NrrRh_TA6UoVUG5Fr09cF3519yGyTYPr-7UWLcc7pSxaTfQPbkaQVw</recordid><startdate>20030701</startdate><enddate>20030701</enddate><creator>Wuyts, W.A</creator><creator>Vanaudenaerde, B.M</creator><creator>Dupont, L.J</creator><creator>Demedts, M.G</creator><creator>Verleden, G.M</creator><general>Eur Respiratory Soc</general><general>Maney</general><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>7X8</scope></search><sort><creationdate>20030701</creationdate><title>N-acetylcysteine reduces chemokine release via inhibition of p38 MAPK in human airway smooth muscle cells</title><author>Wuyts, W.A ; Vanaudenaerde, B.M ; Dupont, L.J ; Demedts, M.G ; Verleden, G.M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-de4657b1fac8e85aa6133381071d98b17184cd92a30f412eb704e6e0f3b3de6d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Acetylcysteine - pharmacology</topic><topic>Asthma - enzymology</topic><topic>Asthma - immunology</topic><topic>Biological and medical sciences</topic><topic>Blotting, Northern</topic><topic>Cells, Cultured</topic><topic>Chemokine CCL11</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Chemokines - metabolism</topic><topic>Chemokines, CC - antagonists & inhibitors</topic><topic>Chemokines, CC - metabolism</topic><topic>Digestive system</topic><topic>Dinoprost - analogs & derivatives</topic><topic>Enzyme Activation</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>F2-Isoprostanes - metabolism</topic><topic>Humans</topic><topic>Interleukin-1 - pharmacology</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>JNK Mitogen-Activated Protein Kinases</topic><topic>MAP Kinase Kinase 4</topic><topic>MAP Kinase Signaling System</topic><topic>Medical sciences</topic><topic>Mitogen-Activated Protein Kinase Kinases</topic><topic>Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Muscle, Smooth - drug effects</topic><topic>Muscle, Smooth - enzymology</topic><topic>Muscle, Smooth - immunology</topic><topic>p38 Mitogen-Activated Protein Kinases</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>Signal Transduction</topic><topic>Statistics, Nonparametric</topic><topic>Stimulation, Chemical</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wuyts, W.A</creatorcontrib><creatorcontrib>Vanaudenaerde, B.M</creatorcontrib><creatorcontrib>Dupont, L.J</creatorcontrib><creatorcontrib>Demedts, M.G</creatorcontrib><creatorcontrib>Verleden, G.M</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>The European respiratory journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wuyts, W.A</au><au>Vanaudenaerde, B.M</au><au>Dupont, L.J</au><au>Demedts, M.G</au><au>Verleden, G.M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>N-acetylcysteine reduces chemokine release via inhibition of p38 MAPK in human airway smooth muscle cells</atitle><jtitle>The European respiratory journal</jtitle><addtitle>Eur Respir J</addtitle><date>2003-07-01</date><risdate>2003</risdate><volume>22</volume><issue>1</issue><spage>43</spage><epage>49</epage><pages>43-49</pages><issn>0903-1936</issn><eissn>1399-3003</eissn><abstract>Reactive oxygen species are involved in the activation of several mitogen-activated protein kinases (MAPKs), key-players in the production of several cytokines. Therefore the current study investigated whether N-acetylcysteine (NAC), an antioxidative agent, inhibits the interleukin (IL)-1beta-induced expression and production of eotaxin and monocyte chemotactic protein (MCP)-1 in human airway smooth muscle cells (HASMC). NAC (10 mM) decreased the expression of eotaxin and MCP-1, by 46 +/- 11% (n=7) and 87 +/- 4% (n=6), respectively; the eotaxin release was inhibited by 75 +/- 5% (n=7), whereas the MCP-1 release was decreased by 69 +/- 41% (n=10). NAC (1 mM) also decreased the IL-1beta-induced activation of p38 MAPK. Compared with unstimulated cells, a four-fold increase in 8-isoprostane production in IL-1beta-stimulated HASMC was observed, which could be inhibited by NAC in a concentration-dependent way, with a maximum inhibition of 39 +/- 12%, with 1 mM NAC. The present study demonstrated that N-acetylcysteine inhibits the interleukin-1beta-induced eotaxin and monocyte chemotactic protein 1 expression and production due to a decreased activation of p38 mitogen-activated protein kinase. This study has also shown that N-acetylcysteine decreases the interleukin-1beta-induced production of reactive oxygen species, as suggested by a reduction in the 8-isoprostane production.</abstract><cop>Leeds</cop><pub>Eur Respiratory Soc</pub><pmid>12882449</pmid><doi>10.1183/09031936.03.00064803</doi><tpages>7</tpages></addata></record> |
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| ispartof | The European respiratory journal, 2003-07, Vol.22 (1), p.43-49 |
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| subjects | Acetylcysteine - pharmacology Asthma - enzymology Asthma - immunology Biological and medical sciences Blotting, Northern Cells, Cultured Chemokine CCL11 Chemokine CCL2 - metabolism Chemokines - metabolism Chemokines, CC - antagonists & inhibitors Chemokines, CC - metabolism Digestive system Dinoprost - analogs & derivatives Enzyme Activation Enzyme-Linked Immunosorbent Assay F2-Isoprostanes - metabolism Humans Interleukin-1 - pharmacology Investigative techniques, diagnostic techniques (general aspects) JNK Mitogen-Activated Protein Kinases MAP Kinase Kinase 4 MAP Kinase Signaling System Medical sciences Mitogen-Activated Protein Kinase Kinases Mitogen-Activated Protein Kinases - antagonists & inhibitors Mitogen-Activated Protein Kinases - metabolism Muscle, Smooth - drug effects Muscle, Smooth - enzymology Muscle, Smooth - immunology p38 Mitogen-Activated Protein Kinases Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Signal Transduction Statistics, Nonparametric Stimulation, Chemical |
| title | N-acetylcysteine reduces chemokine release via inhibition of p38 MAPK in human airway smooth muscle cells |
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