Lipopolysaccharide Cross-Tolerance Delays Platelet-Activating Factor-Induced Sudden Death in Swiss Albino Mice: Involvement of Cyclooxygenase in Cross-Tolerance
Lipopolysaccharide (LPS) signaling through Toll-like receptor-4 (TLR-4) has been implicated in the pathogenesis of many infectious diseases. Some believe that TLR-mediated pathogenicity is due, in part, to the lipid pro-inflammatory mediator platelet-activating factor (PAF), but this has been questi...
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| creator | Jacob, Shancy Petsel Lakshmikanth, Chikkamenahalli Lakshminarayana Chaithra, Vyala Hanumanthareddy Kumari, Titus Ruth Shantha Chen, Chu-Huang McIntyre, Thomas M Marathe, Gopal Kedihitlu |
| description | Lipopolysaccharide (LPS) signaling through Toll-like receptor-4 (TLR-4) has been implicated in the pathogenesis of many infectious diseases. Some believe that TLR-mediated pathogenicity is due, in part, to the lipid pro-inflammatory mediator platelet-activating factor (PAF), but this has been questioned. To test the direct contribution of PAF in endotoxemia in murine models, we injected PAF intraperitoneally into Swiss albino mice in the presence and absence of LPS. PAF alone (5 μg/mouse) caused death within 15-20 min, but this could be prevented by pretreating mice with PAF-receptor (PAF-R) antagonists or PAF-acetylhydrolase (PAF-AH). A low dose of LPS (5 mg/kg body wt) did not impair PAF-induced death, whereas higher doses (10 or 20 mg/kg body wt) delayed death, probably via LPS cross-tolerance. Cross-tolerance occurred only when PAF was injected simultaneously with LPS or within 30 min of LPS injection. Tolerance does not appear to be due to an abundant soluble mediator. Histologic examination of lungs and liver and measurement of circulating TNF-α and IL-10 levels suggested that the inflammatory response is not diminished during cross-tolerance. Interestingly, aspirin, a non-specific cyclooxygenase (COX) inhibitor, partially blocked PAF-induced sudden death, whereas NS-398, a specific COX-2 inhibitor, completely protected mice from the lethal effects of PAF. Both COX inhibitors (at 20 mg/kg body wt) independently amplified the cross-tolerance exerted by higher dose of LPS, suggesting that COX-derived eicosanoids may be involved in these events. Thus, PAF does not seem to have a protective role in endotoxemia, but its effects are delayed by LPS in a COX-sensitive way. These findings are likely to shed light on basic aspects of the endotoxin cross-tolerance occurring in many disease conditions and may offer new opportunities for clinical intervention. |
| doi_str_mv | 10.1371/journal.pone.0153282 |
| format | Article |
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Some believe that TLR-mediated pathogenicity is due, in part, to the lipid pro-inflammatory mediator platelet-activating factor (PAF), but this has been questioned. To test the direct contribution of PAF in endotoxemia in murine models, we injected PAF intraperitoneally into Swiss albino mice in the presence and absence of LPS. PAF alone (5 μg/mouse) caused death within 15-20 min, but this could be prevented by pretreating mice with PAF-receptor (PAF-R) antagonists or PAF-acetylhydrolase (PAF-AH). A low dose of LPS (5 mg/kg body wt) did not impair PAF-induced death, whereas higher doses (10 or 20 mg/kg body wt) delayed death, probably via LPS cross-tolerance. Cross-tolerance occurred only when PAF was injected simultaneously with LPS or within 30 min of LPS injection. Tolerance does not appear to be due to an abundant soluble mediator. Histologic examination of lungs and liver and measurement of circulating TNF-α and IL-10 levels suggested that the inflammatory response is not diminished during cross-tolerance. Interestingly, aspirin, a non-specific cyclooxygenase (COX) inhibitor, partially blocked PAF-induced sudden death, whereas NS-398, a specific COX-2 inhibitor, completely protected mice from the lethal effects of PAF. Both COX inhibitors (at 20 mg/kg body wt) independently amplified the cross-tolerance exerted by higher dose of LPS, suggesting that COX-derived eicosanoids may be involved in these events. Thus, PAF does not seem to have a protective role in endotoxemia, but its effects are delayed by LPS in a COX-sensitive way. These findings are likely to shed light on basic aspects of the endotoxin cross-tolerance occurring in many disease conditions and may offer new opportunities for clinical intervention.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0153282</identifier><identifier>PMID: 27064683</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>1-Alkyl-2-acetylglycerophosphocholine esterase ; Acetylcholinesterase ; Albinism ; Anaphylaxis ; Animal models ; Animals ; Aspirin ; Biochemistry ; Biology and Life Sciences ; Cellular signal transduction ; COX-2 inhibitors ; Cross-tolerance ; Cyclooxygenase Inhibitors - pharmacology ; Cyclooxygenase-2 ; Cyclooxygenases ; Cytokines ; Cytokines - metabolism ; Death ; Death, Sudden - etiology ; Death, Sudden - pathology ; Death, Sudden - prevention & control ; Eicosanoids ; Endotoxemia ; Endotoxemia - etiology ; Endotoxemia - mortality ; Endotoxemia - pathology ; Endotoxemia - prevention & control ; Fatty acids ; Health aspects ; Immune system ; Infectious diseases ; Inflammation ; Inflammatory response ; Injections, Intraperitoneal ; Interleukin 10 ; Lethal effects ; Lipids ; Lipopolysaccharides ; Lipopolysaccharides - pharmacology ; Liver ; Lungs ; Male ; Medicine and Health Sciences ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mortality ; Neutrophils ; Pathogenesis ; Pathogenicity ; Pathogens ; Plasma ; Platelet activating factor ; Platelet Activating Factor - administration & dosage ; Platelet Activating Factor - toxicity ; Platelet Membrane Glycoproteins - metabolism ; Prostaglandin-Endoperoxide Synthases - chemistry ; Prostaglandin-Endoperoxide Synthases - metabolism ; Protective Agents - pharmacology ; Proteins ; Receptors, G-Protein-Coupled - metabolism ; Research and Analysis Methods ; Risk factors ; Rodents ; Sepsis ; Signaling ; Studies ; Sudden death ; Survival Rate ; Toll-like receptors ; Tumor necrosis factor-α</subject><ispartof>PloS one, 2016-04, Vol.11 (4), p.e0153282-e0153282</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Jacob et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Jacob et al 2016 Jacob et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-ac73a78159a0ee95539e6bfd1b30101a47ce324bea2bc00de240225fe4d076a33</citedby><cites>FETCH-LOGICAL-c758t-ac73a78159a0ee95539e6bfd1b30101a47ce324bea2bc00de240225fe4d076a33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4827832/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4827832/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2101,2927,23865,27923,27924,53790,53792,79471,79472</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27064683$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Proost, Paul</contributor><creatorcontrib>Jacob, Shancy Petsel</creatorcontrib><creatorcontrib>Lakshmikanth, Chikkamenahalli Lakshminarayana</creatorcontrib><creatorcontrib>Chaithra, Vyala Hanumanthareddy</creatorcontrib><creatorcontrib>Kumari, Titus Ruth Shantha</creatorcontrib><creatorcontrib>Chen, Chu-Huang</creatorcontrib><creatorcontrib>McIntyre, Thomas M</creatorcontrib><creatorcontrib>Marathe, Gopal Kedihitlu</creatorcontrib><title>Lipopolysaccharide Cross-Tolerance Delays Platelet-Activating Factor-Induced Sudden Death in Swiss Albino Mice: Involvement of Cyclooxygenase in Cross-Tolerance</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Lipopolysaccharide (LPS) signaling through Toll-like receptor-4 (TLR-4) has been implicated in the pathogenesis of many infectious diseases. Some believe that TLR-mediated pathogenicity is due, in part, to the lipid pro-inflammatory mediator platelet-activating factor (PAF), but this has been questioned. To test the direct contribution of PAF in endotoxemia in murine models, we injected PAF intraperitoneally into Swiss albino mice in the presence and absence of LPS. PAF alone (5 μg/mouse) caused death within 15-20 min, but this could be prevented by pretreating mice with PAF-receptor (PAF-R) antagonists or PAF-acetylhydrolase (PAF-AH). A low dose of LPS (5 mg/kg body wt) did not impair PAF-induced death, whereas higher doses (10 or 20 mg/kg body wt) delayed death, probably via LPS cross-tolerance. Cross-tolerance occurred only when PAF was injected simultaneously with LPS or within 30 min of LPS injection. Tolerance does not appear to be due to an abundant soluble mediator. Histologic examination of lungs and liver and measurement of circulating TNF-α and IL-10 levels suggested that the inflammatory response is not diminished during cross-tolerance. Interestingly, aspirin, a non-specific cyclooxygenase (COX) inhibitor, partially blocked PAF-induced sudden death, whereas NS-398, a specific COX-2 inhibitor, completely protected mice from the lethal effects of PAF. Both COX inhibitors (at 20 mg/kg body wt) independently amplified the cross-tolerance exerted by higher dose of LPS, suggesting that COX-derived eicosanoids may be involved in these events. Thus, PAF does not seem to have a protective role in endotoxemia, but its effects are delayed by LPS in a COX-sensitive way. These findings are likely to shed light on basic aspects of the endotoxin cross-tolerance occurring in many disease conditions and may offer new opportunities for clinical intervention.</description><subject>1-Alkyl-2-acetylglycerophosphocholine esterase</subject><subject>Acetylcholinesterase</subject><subject>Albinism</subject><subject>Anaphylaxis</subject><subject>Animal models</subject><subject>Animals</subject><subject>Aspirin</subject><subject>Biochemistry</subject><subject>Biology and Life Sciences</subject><subject>Cellular signal transduction</subject><subject>COX-2 inhibitors</subject><subject>Cross-tolerance</subject><subject>Cyclooxygenase Inhibitors - pharmacology</subject><subject>Cyclooxygenase-2</subject><subject>Cyclooxygenases</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Death</subject><subject>Death, Sudden - etiology</subject><subject>Death, Sudden - pathology</subject><subject>Death, Sudden - prevention & control</subject><subject>Eicosanoids</subject><subject>Endotoxemia</subject><subject>Endotoxemia - etiology</subject><subject>Endotoxemia - mortality</subject><subject>Endotoxemia - pathology</subject><subject>Endotoxemia - prevention & control</subject><subject>Fatty acids</subject><subject>Health aspects</subject><subject>Immune system</subject><subject>Infectious diseases</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Injections, Intraperitoneal</subject><subject>Interleukin 10</subject><subject>Lethal effects</subject><subject>Lipids</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Liver</subject><subject>Lungs</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C57BL</subject><subject>Mortality</subject><subject>Neutrophils</subject><subject>Pathogenesis</subject><subject>Pathogenicity</subject><subject>Pathogens</subject><subject>Plasma</subject><subject>Platelet activating factor</subject><subject>Platelet Activating Factor - administration & dosage</subject><subject>Platelet Activating Factor - toxicity</subject><subject>Platelet Membrane Glycoproteins - metabolism</subject><subject>Prostaglandin-Endoperoxide Synthases - chemistry</subject><subject>Prostaglandin-Endoperoxide Synthases - metabolism</subject><subject>Protective Agents - pharmacology</subject><subject>Proteins</subject><subject>Receptors, G-Protein-Coupled - metabolism</subject><subject>Research and Analysis Methods</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Sepsis</subject><subject>Signaling</subject><subject>Studies</subject><subject>Sudden death</subject><subject>Survival Rate</subject><subject>Toll-like receptors</subject><subject>Tumor 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Cross-Tolerance Delays Platelet-Activating Factor-Induced Sudden Death in Swiss Albino Mice: Involvement of Cyclooxygenase in Cross-Tolerance</title><author>Jacob, Shancy Petsel ; Lakshmikanth, Chikkamenahalli Lakshminarayana ; Chaithra, Vyala Hanumanthareddy ; Kumari, Titus Ruth Shantha ; Chen, Chu-Huang ; McIntyre, Thomas M ; Marathe, Gopal Kedihitlu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-ac73a78159a0ee95539e6bfd1b30101a47ce324bea2bc00de240225fe4d076a33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>1-Alkyl-2-acetylglycerophosphocholine esterase</topic><topic>Acetylcholinesterase</topic><topic>Albinism</topic><topic>Anaphylaxis</topic><topic>Animal models</topic><topic>Animals</topic><topic>Aspirin</topic><topic>Biochemistry</topic><topic>Biology and Life Sciences</topic><topic>Cellular signal transduction</topic><topic>COX-2 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Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jacob, Shancy Petsel</au><au>Lakshmikanth, Chikkamenahalli Lakshminarayana</au><au>Chaithra, Vyala Hanumanthareddy</au><au>Kumari, Titus Ruth Shantha</au><au>Chen, Chu-Huang</au><au>McIntyre, Thomas M</au><au>Marathe, Gopal Kedihitlu</au><au>Proost, Paul</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lipopolysaccharide Cross-Tolerance Delays Platelet-Activating Factor-Induced Sudden Death in Swiss Albino Mice: Involvement of Cyclooxygenase in Cross-Tolerance</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-04-11</date><risdate>2016</risdate><volume>11</volume><issue>4</issue><spage>e0153282</spage><epage>e0153282</epage><pages>e0153282-e0153282</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Lipopolysaccharide (LPS) signaling through Toll-like receptor-4 (TLR-4) has been implicated in the pathogenesis of many infectious diseases. Some believe that TLR-mediated pathogenicity is due, in part, to the lipid pro-inflammatory mediator platelet-activating factor (PAF), but this has been questioned. To test the direct contribution of PAF in endotoxemia in murine models, we injected PAF intraperitoneally into Swiss albino mice in the presence and absence of LPS. PAF alone (5 μg/mouse) caused death within 15-20 min, but this could be prevented by pretreating mice with PAF-receptor (PAF-R) antagonists or PAF-acetylhydrolase (PAF-AH). A low dose of LPS (5 mg/kg body wt) did not impair PAF-induced death, whereas higher doses (10 or 20 mg/kg body wt) delayed death, probably via LPS cross-tolerance. Cross-tolerance occurred only when PAF was injected simultaneously with LPS or within 30 min of LPS injection. Tolerance does not appear to be due to an abundant soluble mediator. Histologic examination of lungs and liver and measurement of circulating TNF-α and IL-10 levels suggested that the inflammatory response is not diminished during cross-tolerance. Interestingly, aspirin, a non-specific cyclooxygenase (COX) inhibitor, partially blocked PAF-induced sudden death, whereas NS-398, a specific COX-2 inhibitor, completely protected mice from the lethal effects of PAF. Both COX inhibitors (at 20 mg/kg body wt) independently amplified the cross-tolerance exerted by higher dose of LPS, suggesting that COX-derived eicosanoids may be involved in these events. Thus, PAF does not seem to have a protective role in endotoxemia, but its effects are delayed by LPS in a COX-sensitive way. These findings are likely to shed light on basic aspects of the endotoxin cross-tolerance occurring in many disease conditions and may offer new opportunities for clinical intervention.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27064683</pmid><doi>10.1371/journal.pone.0153282</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2016-04, Vol.11 (4), p.e0153282-e0153282 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1780143111 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 1-Alkyl-2-acetylglycerophosphocholine esterase Acetylcholinesterase Albinism Anaphylaxis Animal models Animals Aspirin Biochemistry Biology and Life Sciences Cellular signal transduction COX-2 inhibitors Cross-tolerance Cyclooxygenase Inhibitors - pharmacology Cyclooxygenase-2 Cyclooxygenases Cytokines Cytokines - metabolism Death Death, Sudden - etiology Death, Sudden - pathology Death, Sudden - prevention & control Eicosanoids Endotoxemia Endotoxemia - etiology Endotoxemia - mortality Endotoxemia - pathology Endotoxemia - prevention & control Fatty acids Health aspects Immune system Infectious diseases Inflammation Inflammatory response Injections, Intraperitoneal Interleukin 10 Lethal effects Lipids Lipopolysaccharides Lipopolysaccharides - pharmacology Liver Lungs Male Medicine and Health Sciences Mice Mice, Inbred BALB C Mice, Inbred C57BL Mortality Neutrophils Pathogenesis Pathogenicity Pathogens Plasma Platelet activating factor Platelet Activating Factor - administration & dosage Platelet Activating Factor - toxicity Platelet Membrane Glycoproteins - metabolism Prostaglandin-Endoperoxide Synthases - chemistry Prostaglandin-Endoperoxide Synthases - metabolism Protective Agents - pharmacology Proteins Receptors, G-Protein-Coupled - metabolism Research and Analysis Methods Risk factors Rodents Sepsis Signaling Studies Sudden death Survival Rate Toll-like receptors Tumor necrosis factor-α |
| title | Lipopolysaccharide Cross-Tolerance Delays Platelet-Activating Factor-Induced Sudden Death in Swiss Albino Mice: Involvement of Cyclooxygenase in Cross-Tolerance |
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