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Immunomodulatory approaches in managing lung inflammation in COVID‐19: A double‐edge sword

INTRODUCTION: The novel coronavirus infectious disease 2019 (COVID‐19) which is caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) has emerged as a gigantic problem. The lung is the major target organ of SARS‐CoV‐2 and some of its variants like Delta and Omicron variant adapted i...

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Autores principales: Verma, Geetika, Dhawan, Manish, Saied, AbdulRahman A., Kaur, Geetika, Kumar, Reetesh, Emran, Talha Bin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10521379/
https://www.ncbi.nlm.nih.gov/pubmed/37773723
http://dx.doi.org/10.1002/iid3.1020
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author Verma, Geetika
Dhawan, Manish
Saied, AbdulRahman A.
Kaur, Geetika
Kumar, Reetesh
Emran, Talha Bin
author_facet Verma, Geetika
Dhawan, Manish
Saied, AbdulRahman A.
Kaur, Geetika
Kumar, Reetesh
Emran, Talha Bin
author_sort Verma, Geetika
collection PubMed
description INTRODUCTION: The novel coronavirus infectious disease 2019 (COVID‐19) which is caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) has emerged as a gigantic problem. The lung is the major target organ of SARS‐CoV‐2 and some of its variants like Delta and Omicron variant adapted in such a way that these variants can significantly damage this vital organ of the body. These variants raised a few eyebrows as the outbreaks have been seen in the vaccinated population. Patients develop severe respiratory illnesses which eventually prove fatal unless treated early. MAIN BODY: Studies have shown that SARS‐CoV‐2 causes the release of pro‐inflammatory cytokines such as interleukin (IL)‐6, IL‐1β and tumor necrosis factor (TNF)‐α which are mediators of lung inflammation, lung damage, fever, and fibrosis. Additionally, various chemokines have been found to play an important role in the disease progression. A plethora of pro‐inflammatory cytokines “cytokine storm” has been observed in severe cases of SARS‐CoV‐2 infection leading to acute respiratory distress syndrome (ARDS) and pneumonia that may prove fatal. To counteract cytokine storm‐inducing lung inflammation, several promising immunomodulatory approaches are being investigated in numerous clinical trials. However, the benefits of using these strategies should outweigh the risks involved as the use of certain immunosuppressive approaches might lead the host susceptible to secondary bacterial infections. CONCLUSION: The present review discusses promising immunomodulatory approaches to manage lung inflammation in COVID‐19 cases which may serve as potential therapeutic options in the future and may prove lifesaving.
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spelling pubmed-105213792023-09-27 Immunomodulatory approaches in managing lung inflammation in COVID‐19: A double‐edge sword Verma, Geetika Dhawan, Manish Saied, AbdulRahman A. Kaur, Geetika Kumar, Reetesh Emran, Talha Bin Immun Inflamm Dis Review Articles INTRODUCTION: The novel coronavirus infectious disease 2019 (COVID‐19) which is caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) has emerged as a gigantic problem. The lung is the major target organ of SARS‐CoV‐2 and some of its variants like Delta and Omicron variant adapted in such a way that these variants can significantly damage this vital organ of the body. These variants raised a few eyebrows as the outbreaks have been seen in the vaccinated population. Patients develop severe respiratory illnesses which eventually prove fatal unless treated early. MAIN BODY: Studies have shown that SARS‐CoV‐2 causes the release of pro‐inflammatory cytokines such as interleukin (IL)‐6, IL‐1β and tumor necrosis factor (TNF)‐α which are mediators of lung inflammation, lung damage, fever, and fibrosis. Additionally, various chemokines have been found to play an important role in the disease progression. A plethora of pro‐inflammatory cytokines “cytokine storm” has been observed in severe cases of SARS‐CoV‐2 infection leading to acute respiratory distress syndrome (ARDS) and pneumonia that may prove fatal. To counteract cytokine storm‐inducing lung inflammation, several promising immunomodulatory approaches are being investigated in numerous clinical trials. However, the benefits of using these strategies should outweigh the risks involved as the use of certain immunosuppressive approaches might lead the host susceptible to secondary bacterial infections. CONCLUSION: The present review discusses promising immunomodulatory approaches to manage lung inflammation in COVID‐19 cases which may serve as potential therapeutic options in the future and may prove lifesaving. John Wiley and Sons Inc. 2023-09-26 /pmc/articles/PMC10521379/ /pubmed/37773723 http://dx.doi.org/10.1002/iid3.1020 Text en © 2023 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Articles
Verma, Geetika
Dhawan, Manish
Saied, AbdulRahman A.
Kaur, Geetika
Kumar, Reetesh
Emran, Talha Bin
Immunomodulatory approaches in managing lung inflammation in COVID‐19: A double‐edge sword
title Immunomodulatory approaches in managing lung inflammation in COVID‐19: A double‐edge sword
title_full Immunomodulatory approaches in managing lung inflammation in COVID‐19: A double‐edge sword
title_fullStr Immunomodulatory approaches in managing lung inflammation in COVID‐19: A double‐edge sword
title_full_unstemmed Immunomodulatory approaches in managing lung inflammation in COVID‐19: A double‐edge sword
title_short Immunomodulatory approaches in managing lung inflammation in COVID‐19: A double‐edge sword
title_sort immunomodulatory approaches in managing lung inflammation in covid‐19: a double‐edge sword
topic Review Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10521379/
https://www.ncbi.nlm.nih.gov/pubmed/37773723
http://dx.doi.org/10.1002/iid3.1020
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