دورية أكاديمية
أعرض في EDS

Absorption of PCB126 by upper airways impairs G protein-coupled receptor-mediated immune response.

التفاصيل البيبلوغرافية
العنوان: Absorption of PCB126 by upper airways impairs G protein-coupled receptor-mediated immune response.
المؤلفون: Shimada AL; Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-900 Brazil., Cruz WS; Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-900 Brazil., Loiola RA; Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-900 Brazil., Drewes CC; Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-900 Brazil., Dörr F; Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-900 Brazil., Figueiredo NG; Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-900 Brazil., Pinto E; Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-900 Brazil., Farsky SH; Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-900 Brazil.
المصدر: Scientific reports [Sci Rep] 2015 Oct 09; Vol. 5, pp. 14917. Date of Electronic Publication: 2015 Oct 09.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 101563288 Publication Model: Electronic Cited Medium: Internet ISSN: 2045-2322 (Electronic) Linking ISSN: 20452322 NLM ISO Abbreviation: Sci Rep Subsets: MEDLINE
أسماء مطبوعة: Original Publication: London : Nature Publishing Group, copyright 2011-
مواضيع طبية MeSH: Immunity, Innate/*drug effects , Polychlorinated Biphenyls/*toxicity , Receptors, G-Protein-Coupled/*metabolism , Respiratory System/*drug effects, Adipose Tissue/drug effects ; Adipose Tissue/immunology ; Adipose Tissue/metabolism ; Administration, Intranasal ; Animals ; Blotting, Western ; Cell Adhesion Molecules/blood ; Enzyme-Linked Immunosorbent Assay ; Kidney/drug effects ; Kidney/immunology ; Kidney/metabolism ; Liver/drug effects ; Liver/immunology ; Liver/metabolism ; Lung/drug effects ; Lung/immunology ; Lung/metabolism ; Male ; Nasal Absorption ; Neutrophils/drug effects ; Neutrophils/metabolism ; Polychlorinated Biphenyls/administration & dosage ; Polychlorinated Biphenyls/pharmacokinetics ; Rats, Wistar ; Receptors, Aryl Hydrocarbon/metabolism ; Respiratory Burst/drug effects ; Respiratory System/immunology ; Respiratory System/metabolism
مستخلص: PCB126 is a dioxin-like polychlorinated biphenyl (PCB) environmental pollutant with a significant impact on human health, as it bioaccumulates and causes severe toxicity. PCB126-induced immune toxicity has been described, although the mechanisms have not been fully elucidated. In this study, an in vivo protocol of PCB126 intoxication into male Wistar rats by intranasal route was used, which has not yet been described. The intoxication was characterised by PCB126 accumulation in the lungs and liver, and enhanced aryl hydrocarbon receptor expression in the liver, lungs, kidneys, and adipose tissues. Moreover, an innate immune deficiency was characterised by impairment of adhesion receptors on blood leukocytes and by reduced blood neutrophil locomotion and oxidative burst activation elicited by ex vivo G protein-coupled receptor (GPCR) activation. Specificity of PCB126 actions on the GPCR pathway was shown by normal burst oxidative activation evoked by Toll-like receptor 4 and protein kinase C direct activation. Moreover, in vivo PCB180 intoxication did not alter adhesion receptors on blood leukocytes either blood neutrophil locomotion, and only partially reduced the GPCR-induced burst oxidative activation on neutrophils. Therefore, a novel mechanism of in vivo PCB126 toxicity is described which impairs a pivotal inflammatory pathway to the host defence against infections.
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المشرفين على المادة: 0 (Cell Adhesion Molecules)
0 (Receptors, Aryl Hydrocarbon)
0 (Receptors, G-Protein-Coupled)
DFC2HB4I0K (Polychlorinated Biphenyls)
TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
تواريخ الأحداث: Date Created: 20151010 Date Completed: 20160817 Latest Revision: 20181113
رمز التحديث: 20240829
مُعرف محوري في PubMed: PMC4598834
DOI: 10.1038/srep14917
PMID: 26449762
قاعدة البيانات: MEDLINE
الوصف
تدمد:2045-2322
DOI:10.1038/srep14917