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MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile
The Middle East respiratory syndrome coronavirus (MERS-CoV) has been recognized as a highly pathogenic virus to humans that infects the respiratory tract and is associated with high morbidity and mortality. Studies in animal models suggest that MERS-CoV infection induces a strong inflammatory respon...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier Ltd.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7129230/ https://www.ncbi.nlm.nih.gov/pubmed/29414327 http://dx.doi.org/10.1016/j.cyto.2018.01.025 |
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author | Mahallawi, Waleed H. Khabour, Omar F. Zhang, Qibo Makhdoum, Hatim M. Suliman, Bandar A. |
author_facet | Mahallawi, Waleed H. Khabour, Omar F. Zhang, Qibo Makhdoum, Hatim M. Suliman, Bandar A. |
author_sort | Mahallawi, Waleed H. |
collection | PubMed |
description | The Middle East respiratory syndrome coronavirus (MERS-CoV) has been recognized as a highly pathogenic virus to humans that infects the respiratory tract and is associated with high morbidity and mortality. Studies in animal models suggest that MERS-CoV infection induces a strong inflammatory response, which may be related to the severity of disease. Data showing the cytokine profiles in humans during the acute phase of MERS-CoV infection are limited. In this study, we have analyzed the profile of cytokine responses in plasma samples from patients with confirmed MERS-CoV infections (n = 7) compared to healthy controls (n = 13). The cytokine profiles, including T helper (Th) 1, Th2 and Th17 responses, were analyzed using cytometric bead array (CBA). A prominent pro-inflammatory Th1 and Th17 response was clearly seen in patients with MERS-CoV infection, with markedly increased concentrations of IFN-γ, TNF-α, IL-15 and IL-17 compared to controls. IL-12 expression levels showed no difference between patients with MERS-CoV infection and the healthy controls despite the significantly increased levels of IFN-α2 and IFN-γ (P < .01). No changes were observed in the levels of IL-2, IL-4, IL-5, IL-13, and TGF-α (P > .05). Our results demonstrate a marked pro-inflammatory cytokine response during the acute phase of MERS-CoV infection in humans. |
format | Online Article Text |
id | pubmed-7129230 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Elsevier Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-71292302020-04-08 MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile Mahallawi, Waleed H. Khabour, Omar F. Zhang, Qibo Makhdoum, Hatim M. Suliman, Bandar A. Cytokine Article The Middle East respiratory syndrome coronavirus (MERS-CoV) has been recognized as a highly pathogenic virus to humans that infects the respiratory tract and is associated with high morbidity and mortality. Studies in animal models suggest that MERS-CoV infection induces a strong inflammatory response, which may be related to the severity of disease. Data showing the cytokine profiles in humans during the acute phase of MERS-CoV infection are limited. In this study, we have analyzed the profile of cytokine responses in plasma samples from patients with confirmed MERS-CoV infections (n = 7) compared to healthy controls (n = 13). The cytokine profiles, including T helper (Th) 1, Th2 and Th17 responses, were analyzed using cytometric bead array (CBA). A prominent pro-inflammatory Th1 and Th17 response was clearly seen in patients with MERS-CoV infection, with markedly increased concentrations of IFN-γ, TNF-α, IL-15 and IL-17 compared to controls. IL-12 expression levels showed no difference between patients with MERS-CoV infection and the healthy controls despite the significantly increased levels of IFN-α2 and IFN-γ (P < .01). No changes were observed in the levels of IL-2, IL-4, IL-5, IL-13, and TGF-α (P > .05). Our results demonstrate a marked pro-inflammatory cytokine response during the acute phase of MERS-CoV infection in humans. Elsevier Ltd. 2018-04 2018-02-02 /pmc/articles/PMC7129230/ /pubmed/29414327 http://dx.doi.org/10.1016/j.cyto.2018.01.025 Text en © 2018 Elsevier Ltd. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. |
spellingShingle | Article Mahallawi, Waleed H. Khabour, Omar F. Zhang, Qibo Makhdoum, Hatim M. Suliman, Bandar A. MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile |
title | MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile |
title_full | MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile |
title_fullStr | MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile |
title_full_unstemmed | MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile |
title_short | MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile |
title_sort | mers-cov infection in humans is associated with a pro-inflammatory th1 and th17 cytokine profile |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7129230/ https://www.ncbi.nlm.nih.gov/pubmed/29414327 http://dx.doi.org/10.1016/j.cyto.2018.01.025 |
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