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Aryl hydrocarbon receptor (AHR) functions in infectious and sterile inflammation and NAD(+)-dependent metabolic adaptation
Aryl hydrocarbon receptor (AHR) research has shifted from exploring dioxin toxicity to elucidation of various physiologic AHR functions. Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is known to exert cellular stress-mediated sterile inflammatory responses in exposed human tissues but may b...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Springer Berlin Heidelberg
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8461142/ https://www.ncbi.nlm.nih.gov/pubmed/34559251 http://dx.doi.org/10.1007/s00204-021-03134-9 |
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author | Bock, Karl Walter |
author_facet | Bock, Karl Walter |
author_sort | Bock, Karl Walter |
collection | PubMed |
description | Aryl hydrocarbon receptor (AHR) research has shifted from exploring dioxin toxicity to elucidation of various physiologic AHR functions. Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is known to exert cellular stress-mediated sterile inflammatory responses in exposed human tissues but may be lethal in sensitive species. Inflammation can be thought of as the extreme end of a spectrum ranging from homeostasis to stress responses (sterile inflammation) and to defense against infection (infectious inflammation). Defense against bacterial infection by generation of reactive oxygen species has to be strictly controlled and may use up a considerable amount of energy. NAD(+)-mediated energy metabolism adapts to various inflammatory responses. As examples, the present commentary tries to integrate responses of AHR and NAD(+)-consuming enzymes (PARP7/TiPARP, CD38 and sirtuins) into infectious and stress-induced inflammatory responses, the latter exemplified by nonalcoholic fatty liver disease (NAFLD). TCDD toxicity models in sensitive species provide hints to molecular AHR targets of energy metabolism including gluconeogenesis and glycolysis. AHR research remains challenging and promising. |
format | Online Article Text |
id | pubmed-8461142 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Springer Berlin Heidelberg |
record_format | MEDLINE/PubMed |
spelling | pubmed-84611422021-09-24 Aryl hydrocarbon receptor (AHR) functions in infectious and sterile inflammation and NAD(+)-dependent metabolic adaptation Bock, Karl Walter Arch Toxicol Review Article Aryl hydrocarbon receptor (AHR) research has shifted from exploring dioxin toxicity to elucidation of various physiologic AHR functions. Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is known to exert cellular stress-mediated sterile inflammatory responses in exposed human tissues but may be lethal in sensitive species. Inflammation can be thought of as the extreme end of a spectrum ranging from homeostasis to stress responses (sterile inflammation) and to defense against infection (infectious inflammation). Defense against bacterial infection by generation of reactive oxygen species has to be strictly controlled and may use up a considerable amount of energy. NAD(+)-mediated energy metabolism adapts to various inflammatory responses. As examples, the present commentary tries to integrate responses of AHR and NAD(+)-consuming enzymes (PARP7/TiPARP, CD38 and sirtuins) into infectious and stress-induced inflammatory responses, the latter exemplified by nonalcoholic fatty liver disease (NAFLD). TCDD toxicity models in sensitive species provide hints to molecular AHR targets of energy metabolism including gluconeogenesis and glycolysis. AHR research remains challenging and promising. Springer Berlin Heidelberg 2021-09-24 2021 /pmc/articles/PMC8461142/ /pubmed/34559251 http://dx.doi.org/10.1007/s00204-021-03134-9 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Review Article Bock, Karl Walter Aryl hydrocarbon receptor (AHR) functions in infectious and sterile inflammation and NAD(+)-dependent metabolic adaptation |
title | Aryl hydrocarbon receptor (AHR) functions in infectious and sterile inflammation and NAD(+)-dependent metabolic adaptation |
title_full | Aryl hydrocarbon receptor (AHR) functions in infectious and sterile inflammation and NAD(+)-dependent metabolic adaptation |
title_fullStr | Aryl hydrocarbon receptor (AHR) functions in infectious and sterile inflammation and NAD(+)-dependent metabolic adaptation |
title_full_unstemmed | Aryl hydrocarbon receptor (AHR) functions in infectious and sterile inflammation and NAD(+)-dependent metabolic adaptation |
title_short | Aryl hydrocarbon receptor (AHR) functions in infectious and sterile inflammation and NAD(+)-dependent metabolic adaptation |
title_sort | aryl hydrocarbon receptor (ahr) functions in infectious and sterile inflammation and nad(+)-dependent metabolic adaptation |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8461142/ https://www.ncbi.nlm.nih.gov/pubmed/34559251 http://dx.doi.org/10.1007/s00204-021-03134-9 |
work_keys_str_mv | AT bockkarlwalter arylhydrocarbonreceptorahrfunctionsininfectiousandsterileinflammationandnaddependentmetabolicadaptation |