N-acetyl-L-cysteine (NAC) inhibits virus replication and expression of pro-inflammatory molecules in A549 cells infected with highly pathogenic H5N1 influenza A virus
Identifieur interne : 000413 ( Hal/Corpus ); précédent : 000412; suivant : 000414N-acetyl-L-cysteine (NAC) inhibits virus replication and expression of pro-inflammatory molecules in A549 cells infected with highly pathogenic H5N1 influenza A virus
Auteurs : Janina Geiler ; Martin Michaelis ; Patrizia Naczk ; Anke Leutz ; Klaus Langer ; Hans-Wilhelm Doerr ; Jindrich CinatlSource :
- Biochemical Pharmacology [ 0006-2952 ] ; 2009-11-21.
Abstract
The antioxidant N-acetyl-L-cysteine (NAC) had been shown to inhibit replication of seasonal human influenza A viruses. Here, the effects of NAC on virus replication, virus-induced pro-inflammatory responses and virus-induced apoptosis were investigated in H5N1-infected lung epithelial (A549) cells. NAC at concentrations ranging from 5 to 15mM reduced H5N1-induced cytopathogenic effects (CPE), virus-induced apoptosis and infectious viral yields 24hours post-infection. NAC also decreased the production of pro-inflammatory molecules (CXCL8, CXCL10, CCL5, interleukin-6 (IL-6)) in H5N1-infected A549 cells and reduced monocyte migration towards supernatants of H5N1-infected A549 cells. The antiviral and anti-inflammatory mechanisms of NAC included inhibition of activation of oxidant sensitive pathways including transcription factor NF-κB and mitogen activated protein kinase p38. Pharmacological inhibitors of NF-κB (BAY 11-7085) or p38 (SB203580) exerted similar effects like those determined for NAC in H5N1-infected cells. The combination of BAY 11-7085 and SB203580 resulted in increased inhibitory effects on virus replication and production of pro-inflammatory molecules relative to either single treatment. NAC inhibits H5N1 replication and H5N1-induced production of pro-inflammatory molecules. Therefore, antioxidants like NAC represent a potential additional treatment option that could be considered in the case of an influenza A virus pandemic.
Url:
DOI: 10.1016/j.bcp.2009.08.025
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Here, the effects of NAC on virus replication, virus-induced pro-inflammatory responses and virus-induced apoptosis were investigated in H5N1-infected lung epithelial (A549) cells. NAC at concentrations ranging from 5 to 15mM reduced H5N1-induced cytopathogenic effects (CPE), virus-induced apoptosis and infectious viral yields 24hours post-infection. NAC also decreased the production of pro-inflammatory molecules (CXCL8, CXCL10, CCL5, interleukin-6 (IL-6)) in H5N1-infected A549 cells and reduced monocyte migration towards supernatants of H5N1-infected A549 cells. The antiviral and anti-inflammatory mechanisms of NAC included inhibition of activation of oxidant sensitive pathways including transcription factor NF-κB and mitogen activated protein kinase p38. Pharmacological inhibitors of NF-κB (BAY 11-7085) or p38 (SB203580) exerted similar effects like those determined for NAC in H5N1-infected cells. The combination of BAY 11-7085 and SB203580 resulted in increased inhibitory effects on virus replication and production of pro-inflammatory molecules relative to either single treatment. NAC inhibits H5N1 replication and H5N1-induced production of pro-inflammatory molecules. Therefore, antioxidants like NAC represent a potential additional treatment option that could be considered in the case of an influenza A virus pandemic.</p> </div></front></TEI><hal api="V3"> <titleStmt> <title xml:lang="en">N-acetyl-L-cysteine (NAC) inhibits virus replication and expression of pro-inflammatory molecules in A549 cells infected with highly pathogenic H5N1 influenza A virus</title> <author role="aut"> <persName> <forename type="first">Janina</forename> <surname>Geiler</surname> </persName> <idno type="halauthorid">547269</idno> </author> <author role="aut"> <persName> <forename type="first">Martin</forename> <surname>Michaelis</surname> </persName> <idno type="halauthorid">547226</idno> </author> <author role="aut"> <persName> <forename type="first">Patrizia</forename> <surname>Naczk</surname> </persName> <idno type="halauthorid">549223</idno> </author> <author role="aut"> <persName> <forename type="first">Anke</forename> <surname>Leutz</surname> </persName> <idno 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type="md5">3e039be0ba83a5dd992f59ce23acd0bf</email> <email type="domain">em.uni-frankfurt.de</email> <idno type="halauthorid">547228</idno> </author> </analytic> <monogr> <idno type="halJournalId" status="VALID">11103</idno> <idno type="issn">0006-2952</idno> <idno type="eissn">1873-2968</idno> <title level="j">Biochemical Pharmacology</title> <imprint> <publisher>Elsevier</publisher> <biblScope unit="volume">79</biblScope> <biblScope unit="issue">3</biblScope> <biblScope unit="pp">413</biblScope> <date type="datePub">2009-11-21</date> </imprint> </monogr> <idno type="doi">10.1016/j.bcp.2009.08.025</idno> </biblStruct> </sourceDesc> <profileDesc> <langUsage> <language ident="en">English</language> </langUsage> <textClass> <keywords scheme="author"> <term xml:lang="lt">ROS</term> <term xml:lang="lt">NAC</term> <term xml:lang="lt">cytokines</term> <term xml:lang="lt">H5N1</term> <term xml:lang="lt">apoptosis</term> </keywords> <classCode scheme="halTypology" n="ART">Journal articles</classCode> </textClass> <abstract xml:lang="en"> <p>The antioxidant N-acetyl-L-cysteine (NAC) had been shown to inhibit replication of seasonal human influenza A viruses. Here, the effects of NAC on virus replication, virus-induced pro-inflammatory responses and virus-induced apoptosis were investigated in H5N1-infected lung epithelial (A549) cells. NAC at concentrations ranging from 5 to 15mM reduced H5N1-induced cytopathogenic effects (CPE), virus-induced apoptosis and infectious viral yields 24hours post-infection. NAC also decreased the production of pro-inflammatory molecules (CXCL8, CXCL10, CCL5, interleukin-6 (IL-6)) in H5N1-infected A549 cells and reduced monocyte migration towards supernatants of H5N1-infected A549 cells. The antiviral and anti-inflammatory mechanisms of NAC included inhibition of activation of oxidant sensitive pathways including transcription factor NF-κB and mitogen activated protein kinase p38. Pharmacological inhibitors of NF-κB (BAY 11-7085) or p38 (SB203580) exerted similar effects like those determined for NAC in H5N1-infected cells. The combination of BAY 11-7085 and SB203580 resulted in increased inhibitory effects on virus replication and production of pro-inflammatory molecules relative to either single treatment. NAC inhibits H5N1 replication and H5N1-induced production of pro-inflammatory molecules. Therefore, antioxidants like NAC represent a potential additional treatment option that could be considered in the case of an influenza A virus pandemic.</p> </abstract> </profileDesc> </hal></record>Pour manipuler ce document sous Unix (Dilib)
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