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A possible link between recurrent upper respiratory tract infections and lower cytokine production in patients with Q fever fatigue syndrome
Besides fatigue, many Q fever fatigue syndrome (QFS) patients also complain of frequently recurring upper respiratory tract infections with severe symptoms. We investigated whether immunologic dysregulation contributes to these complaints. Cytokine and chemokine production was measured after stimula...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7163623/ https://www.ncbi.nlm.nih.gov/pubmed/31001808 http://dx.doi.org/10.1002/eji.201848012 |
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author | Raijmakers, Ruud P.H. Jansen, Anne F.M. Keijmel, Stephan P. van der Meer, Jos W.M. Joosten, Leo A.B. Netea, Mihai G. Bleeker‐Rovers, Chantal P. |
author_facet | Raijmakers, Ruud P.H. Jansen, Anne F.M. Keijmel, Stephan P. van der Meer, Jos W.M. Joosten, Leo A.B. Netea, Mihai G. Bleeker‐Rovers, Chantal P. |
author_sort | Raijmakers, Ruud P.H. |
collection | PubMed |
description | Besides fatigue, many Q fever fatigue syndrome (QFS) patients also complain of frequently recurring upper respiratory tract infections with severe symptoms. We investigated whether immunologic dysregulation contributes to these complaints. Cytokine and chemokine production was measured after stimulating monocytes of QFS patients and age‐ and sex‐matched healthy controls with LPS and several viral ligands. The H3K4me3 mark of open chromatin was measured at the promoter regions of cytokines and chemokines that differed significantly from healthy controls. Monocytes of QFS patients produced significantly less TNF‐α (p = 0.032), IL‐1β (0.004, 0.024, and 0.008), IL‐6 (0.043), RANTES (0.033), IP‐10 (0.049), MCP‐1 (0.022), IL‐ 13 (0.029), and IL‐10 (0.026) than healthy controls when stimulated with various ligands. H3K4me3 expression was significantly lower in QFS patients than in healthy controls on the promoter regions of IL‐1β (p = 0.004), MCP‐1 (<0.001 and <0.001), IP‐10 (<0.001), IL‐10 (0.041), and IL‐13 (<0.001, <0.001, and 0.001). QFS patients showed diminished cytokine responses to various stimuli compared to age‐ and sex‐matched healthy controls, likely due to epigenetic remodeling and long‐term memory as a result from the acute Q fever infection. This might explain the upper respiratory tract ailments in QFS. |
format | Online Article Text |
id | pubmed-7163623 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-71636232020-04-17 A possible link between recurrent upper respiratory tract infections and lower cytokine production in patients with Q fever fatigue syndrome Raijmakers, Ruud P.H. Jansen, Anne F.M. Keijmel, Stephan P. van der Meer, Jos W.M. Joosten, Leo A.B. Netea, Mihai G. Bleeker‐Rovers, Chantal P. Eur J Immunol Innate immunity Besides fatigue, many Q fever fatigue syndrome (QFS) patients also complain of frequently recurring upper respiratory tract infections with severe symptoms. We investigated whether immunologic dysregulation contributes to these complaints. Cytokine and chemokine production was measured after stimulating monocytes of QFS patients and age‐ and sex‐matched healthy controls with LPS and several viral ligands. The H3K4me3 mark of open chromatin was measured at the promoter regions of cytokines and chemokines that differed significantly from healthy controls. Monocytes of QFS patients produced significantly less TNF‐α (p = 0.032), IL‐1β (0.004, 0.024, and 0.008), IL‐6 (0.043), RANTES (0.033), IP‐10 (0.049), MCP‐1 (0.022), IL‐ 13 (0.029), and IL‐10 (0.026) than healthy controls when stimulated with various ligands. H3K4me3 expression was significantly lower in QFS patients than in healthy controls on the promoter regions of IL‐1β (p = 0.004), MCP‐1 (<0.001 and <0.001), IP‐10 (<0.001), IL‐10 (0.041), and IL‐13 (<0.001, <0.001, and 0.001). QFS patients showed diminished cytokine responses to various stimuli compared to age‐ and sex‐matched healthy controls, likely due to epigenetic remodeling and long‐term memory as a result from the acute Q fever infection. This might explain the upper respiratory tract ailments in QFS. John Wiley and Sons Inc. 2019-05-09 2019-07 /pmc/articles/PMC7163623/ /pubmed/31001808 http://dx.doi.org/10.1002/eji.201848012 Text en © 2019 The Authors. European Journal of Immunology published by WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Innate immunity Raijmakers, Ruud P.H. Jansen, Anne F.M. Keijmel, Stephan P. van der Meer, Jos W.M. Joosten, Leo A.B. Netea, Mihai G. Bleeker‐Rovers, Chantal P. A possible link between recurrent upper respiratory tract infections and lower cytokine production in patients with Q fever fatigue syndrome |
title | A possible link between recurrent upper respiratory tract infections and lower cytokine production in patients with Q fever fatigue syndrome |
title_full | A possible link between recurrent upper respiratory tract infections and lower cytokine production in patients with Q fever fatigue syndrome |
title_fullStr | A possible link between recurrent upper respiratory tract infections and lower cytokine production in patients with Q fever fatigue syndrome |
title_full_unstemmed | A possible link between recurrent upper respiratory tract infections and lower cytokine production in patients with Q fever fatigue syndrome |
title_short | A possible link between recurrent upper respiratory tract infections and lower cytokine production in patients with Q fever fatigue syndrome |
title_sort | possible link between recurrent upper respiratory tract infections and lower cytokine production in patients with q fever fatigue syndrome |
topic | Innate immunity |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7163623/ https://www.ncbi.nlm.nih.gov/pubmed/31001808 http://dx.doi.org/10.1002/eji.201848012 |
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