| Autor: |
Khalil BA; Sharjah Institute for Medical Research, College of Medicine, University of Sharjah, Sharjah P.O. Box 27272, United Arab Emirates., Shakartalla SB; Sharjah Institute for Medical Research, College of Medicine, University of Sharjah, Sharjah P.O. Box 27272, United Arab Emirates.; Faculty of Pharmacy, University of Gezira, Wad Medani 2667, Sudan., Goel S; Sharjah Institute for Medical Research, College of Medicine, University of Sharjah, Sharjah P.O. Box 27272, United Arab Emirates., Madkhana B; Sharjah Institute for Medical Research, College of Medicine, University of Sharjah, Sharjah P.O. Box 27272, United Arab Emirates., Halwani R; Sharjah Institute for Medical Research, College of Medicine, University of Sharjah, Sharjah P.O. Box 27272, United Arab Emirates.; College of Medicine, University of Sharjah, Sharjah P.O. Box 27272, United Arab Emirates., Maghazachi AA; Sharjah Institute for Medical Research, College of Medicine, University of Sharjah, Sharjah P.O. Box 27272, United Arab Emirates.; College of Medicine, University of Sharjah, Sharjah P.O. Box 27272, United Arab Emirates., AlSafar H; College of Medicine and Health Sciences, Khalifa University, Abu Dhabi P.O. Box 127788, United Arab Emirates.; Center for Biotechnology, Khalifa University of Science and Technology, Abu Dhabi P.O. Box 127788, United Arab Emirates.; Emirates Bio-Research Center, Ministry of Interior, Abu Dhabi P.O. Box 389, United Arab Emirates., Al-Omari B; College of Medicine and Health Sciences, Khalifa University, Abu Dhabi P.O. Box 127788, United Arab Emirates.; KU Research and Data Intelligence Support Center (RDISC) AW 8474000331, Khalifa University of Science and Technology, Abu Dhabi P.O. Box 127788, United Arab Emirates., Al Bataineh MT; College of Medicine and Health Sciences, Khalifa University, Abu Dhabi P.O. Box 127788, United Arab Emirates.; Center for Biotechnology, Khalifa University of Science and Technology, Abu Dhabi P.O. Box 127788, United Arab Emirates. |
| Abstrakt: |
Acute respiratory distress syndrome (ARDS) is a major complication of the respiratory illness coronavirus disease 2019, with a death rate reaching up to 40%. The main underlying cause of ARDS is a cytokine storm that results in a dysregulated immune response. This review discusses the role of cytokines and chemokines in SARS-CoV-2 and its predecessors SARS-CoV and MERS-CoV, with particular emphasis on the elevated levels of inflammatory mediators that are shown to be correlated with disease severity. For this purpose, we reviewed and analyzed clinical studies, research articles, and reviews published on PubMed, EMBASE, and Web of Science. This review illustrates the role of the innate and adaptive immune responses in SARS, MERS, and COVID-19 and identifies the general cytokine and chemokine profile in each of the three infections, focusing on the most prominent inflammatory mediators primarily responsible for the COVID-19 pathogenesis. The current treatment protocols or medications in clinical trials were reviewed while focusing on those targeting cytokines and chemokines. Altogether, the identified cytokines and chemokines profiles in SARS-CoV, MERS-CoV, and SARS-CoV-2 provide important information to better understand SARS-CoV-2 pathogenesis and highlight the importance of using prominent inflammatory mediators as markers for disease diagnosis and management. Our findings recommend that the use of immunosuppression cocktails provided to patients should be closely monitored and continuously assessed to maintain the desirable effects of cytokines and chemokines needed to fight the SARS, MERS, and COVID-19. The current gap in evidence is the lack of large clinical trials to determine the optimal and effective dosage and timing for a therapeutic regimen. |
