May the Central Nervous System Be Fogged by the Cytokine Storm in COVID-19?: an Appraisal
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LETTER TO THE EDITOR
May the Central Nervous System Be Fogged by the Cytokine Storm in COVID-19?: an Appraisal Yasin Hasan Balcioglu 1
&
Umit Haluk Yesilkaya 1 & Hasan Gokcay 2 & Simge Seren Kirlioglu 1
Received: 27 May 2020 / Accepted: 5 June 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Dear editor: We recently read with interest the article by Acharya et al. entitled “SARS-CoV-2 Infection Leads to Neurological Dysfunction” (Acharya et al. 2020). They have reviewed current literature on the neurological complications and manifestations of COVID-19, however, they were able to identify only a very limited number of studies. In fact, in our latest paper, we have provided a deeper insight on the pathophysiology of the central nervous system involvement of COVID19 and discussed that neuropsychiatric manifestations related COVID-19 might be associated with the involvement of both direct viral transmission and neuroimmune response (Yesilkaya and Balcioglu 2020). Latter includes heightened systemic proinflammatory response which is closely associated with so-called cytokine storm, a well-known phenomenon led by SARS-CoV-2 infection. As viral replication progressively decreases during the latter days of infection, the pathogenesis of COVID-19 has been thought to be predominantly related to an aggressive inflammatory response. Thus, the intense release of proinflammatory cytokines (viz cytokine storm) in the host leads to diffuse alveolar damage, severe hypoxemia, and promotes the development of fatal secondary sepsis (Serrano-Castro et al. 2020). Even though the cytokine storm has been a well-defined condition in many viral infections including influenza and coronavirus (Liu et al. 2016), our appreciation of its effects on the central nervous system (CNS) has remained limited. The primary targets for SARS COV-2 are respiratory epithelial cells and alveolar macrophages. Following the * Yasin Hasan Balcioglu [email protected] 1
Department of Psychiatry, Bakirkoy Prof Mazhar Osman Training and Research Hospital for Psychiatry, Neurology, and Neurosurgery, Istanbul, Turkey
2
Department of Psychiatry, Bagcilar Training and Research Hospital, University of Health Sciences, Istanbul, Turkey
infection of respiratory cells, rapid production and release of many chemokines and cytokines initiate. Macrophages are activated by such proinflammatory chemokines and cytokines, and other key components of the innate immune system, dendritic cells, lead to a more extensive immune response that initiates the cytokine storm. Circulating chemokines attract more inflammatory cells to make them migrate from blood vessels into the site of inflammation, and these cells release additional chemokines/cytokines which amplify cytokine storm (Liu et al. 2016). Although TNF- α, IL-1, and IL-6 are primary cytokines of the acute immune response and the interferons are key cytokines for antiviral immune response, the excessive response of these proinflammatory mediators have been considered major triggers of sep
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