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SARS‐CoV‐2 infection as a trigger of autoimmune response
ABSTRACT: Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID‐19). In this study, we elucidate whether severe acute respiratory syndrome coronavirus disease 2 (SARS‐CoV‐2) stimulates autoantibody production and contribu...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8212749/ https://www.ncbi.nlm.nih.gov/pubmed/33306235 http://dx.doi.org/10.1111/cts.12953 |
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author | Sacchi, Maria C. Tamiazzo, Stefania Stobbione, Paolo Agatea, Lisa De Gaspari, Piera Stecca, Anna Lauritano, Ernesto C. Roveta, Annalisa Tozzoli, Renato Guaschino, Roberto Bonometti, Ramona |
author_facet | Sacchi, Maria C. Tamiazzo, Stefania Stobbione, Paolo Agatea, Lisa De Gaspari, Piera Stecca, Anna Lauritano, Ernesto C. Roveta, Annalisa Tozzoli, Renato Guaschino, Roberto Bonometti, Ramona |
author_sort | Sacchi, Maria C. |
collection | PubMed |
description | ABSTRACT: Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID‐19). In this study, we elucidate whether severe acute respiratory syndrome coronavirus disease 2 (SARS‐CoV‐2) stimulates autoantibody production and contributes to autoimmunity activation. We enrolled 40 adult patients (66.8 years mean age) admitted to Alessandria Hospital between March and April 2020. All the patients had a confirmed COVID‐19 diagnosis and no previously clinical record of autoimmune disease. Forty blood donors were analyzed for the same markers and considered as healthy controls. Our patients had high levels of common inflammatory markers, such as C reactive protein, lactate dehydrogenase, ferritin, and creatinine. Interleukin‐6 concentrations were also increased, supporting the major role of this interleukin during COVID‐19 infection. Lymphocyte numbers were generally lower compared with healthy individuals. All the patients were also screened for the most common autoantibodies. We found a significant prevalence of antinuclear antibodies, antineutrophil cytoplasmic antibodies, and ASCA immunoglobulin A antibodies. We observed that patients having a de novo autoimmune response had the worst acute viral disease prognosis and outcome. Our results sustain the hypothesis that COVID‐19 infection correlates with the autoimmunity markers. Our study might help clinicians to: (a) better understand the heterogeneity of this pathology and (b) correctly evaluate COVID‐19 clinical manifestations. Our data explained why drugs used to treat autoimmune diseases may also be useful for SARS‐CoV‐2 infection. In addition, we highly recommend checking patients with COVID‐19 for autoimmunity markers, mainly when deciding on whether to treat them with plasma transfer therapy. STUDY HIGHLIGHTS: WHAT IS THE CURRENT KNOWLEDGE ON THE TOPIC? WHAT QUESTION DID THIS STUDY ADDRESS? WHAT DOES THIS STUDY ADD TO OUR KNOWLEDGE? HOW MIGHT THIS CHANGE CLINICAL PHARMACOLOGY OR TRANSLATIONAL SCIENCE? ☑ These results suggest that the drugs normally used to treat autoimmune diseases should also be considered during SARS‐CoV‐2, improving public health. In addition, before starting a transfer plasma therapy, it is important to also evaluate the autoimmunity conditions of the patients with COVID‐19. Transferring antibodies or trying to neutralize them should be done with precaution. It is possible that the risk of developing or increasing the autoimmune response may enhance. |
format | Online Article Text |
id | pubmed-8212749 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-82127492021-06-25 SARS‐CoV‐2 infection as a trigger of autoimmune response Sacchi, Maria C. Tamiazzo, Stefania Stobbione, Paolo Agatea, Lisa De Gaspari, Piera Stecca, Anna Lauritano, Ernesto C. Roveta, Annalisa Tozzoli, Renato Guaschino, Roberto Bonometti, Ramona Clin Transl Sci Research ABSTRACT: Currently, few evidences have shown the possible involvement of autoimmunity in patients affected by coronavirus disease 2019 (COVID‐19). In this study, we elucidate whether severe acute respiratory syndrome coronavirus disease 2 (SARS‐CoV‐2) stimulates autoantibody production and contributes to autoimmunity activation. We enrolled 40 adult patients (66.8 years mean age) admitted to Alessandria Hospital between March and April 2020. All the patients had a confirmed COVID‐19 diagnosis and no previously clinical record of autoimmune disease. Forty blood donors were analyzed for the same markers and considered as healthy controls. Our patients had high levels of common inflammatory markers, such as C reactive protein, lactate dehydrogenase, ferritin, and creatinine. Interleukin‐6 concentrations were also increased, supporting the major role of this interleukin during COVID‐19 infection. Lymphocyte numbers were generally lower compared with healthy individuals. All the patients were also screened for the most common autoantibodies. We found a significant prevalence of antinuclear antibodies, antineutrophil cytoplasmic antibodies, and ASCA immunoglobulin A antibodies. We observed that patients having a de novo autoimmune response had the worst acute viral disease prognosis and outcome. Our results sustain the hypothesis that COVID‐19 infection correlates with the autoimmunity markers. Our study might help clinicians to: (a) better understand the heterogeneity of this pathology and (b) correctly evaluate COVID‐19 clinical manifestations. Our data explained why drugs used to treat autoimmune diseases may also be useful for SARS‐CoV‐2 infection. In addition, we highly recommend checking patients with COVID‐19 for autoimmunity markers, mainly when deciding on whether to treat them with plasma transfer therapy. STUDY HIGHLIGHTS: WHAT IS THE CURRENT KNOWLEDGE ON THE TOPIC? WHAT QUESTION DID THIS STUDY ADDRESS? WHAT DOES THIS STUDY ADD TO OUR KNOWLEDGE? HOW MIGHT THIS CHANGE CLINICAL PHARMACOLOGY OR TRANSLATIONAL SCIENCE? ☑ These results suggest that the drugs normally used to treat autoimmune diseases should also be considered during SARS‐CoV‐2, improving public health. In addition, before starting a transfer plasma therapy, it is important to also evaluate the autoimmunity conditions of the patients with COVID‐19. Transferring antibodies or trying to neutralize them should be done with precaution. It is possible that the risk of developing or increasing the autoimmune response may enhance. John Wiley and Sons Inc. 2021-01-21 2021-05 /pmc/articles/PMC8212749/ /pubmed/33306235 http://dx.doi.org/10.1111/cts.12953 Text en © 2020 The Authors. Clinical and Translational Science published by Wiley Periodicals LLC on behalf of the American Society for Clinical Pharmacology and Therapeutics. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Research Sacchi, Maria C. Tamiazzo, Stefania Stobbione, Paolo Agatea, Lisa De Gaspari, Piera Stecca, Anna Lauritano, Ernesto C. Roveta, Annalisa Tozzoli, Renato Guaschino, Roberto Bonometti, Ramona SARS‐CoV‐2 infection as a trigger of autoimmune response |
title | SARS‐CoV‐2 infection as a trigger of autoimmune response |
title_full | SARS‐CoV‐2 infection as a trigger of autoimmune response |
title_fullStr | SARS‐CoV‐2 infection as a trigger of autoimmune response |
title_full_unstemmed | SARS‐CoV‐2 infection as a trigger of autoimmune response |
title_short | SARS‐CoV‐2 infection as a trigger of autoimmune response |
title_sort | sars‐cov‐2 infection as a trigger of autoimmune response |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8212749/ https://www.ncbi.nlm.nih.gov/pubmed/33306235 http://dx.doi.org/10.1111/cts.12953 |
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