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Exp Neurobiol 2021; 30(3): 256-261
Published online June 30, 2021
https://doi.org/10.5607/en21009
© The Korean Society for Brain and Neural Sciences
Sebastián Guartazaca-Guerrero1,2†, Jahir Rodríguez-Morales1,2†, Salma A. Rizo-Téllez3,4, Helena Solleiro-Villavicencio5, Aldo F. Hernández-Valencia2, José Damián Carrillo-Ruiz2,6, Galileo Escobedo3* and Lucía A. Méndez-García3*
1Especialidad en Neurocirugía, Facultad de Medicina, Universidad Nacional Autónoma de México, Coyoacán, Mexico City 04510, 2Neurology and Neurosurgery Unit, General Hospital of Mexico “Dr. Eduardo Liceaga”, Mexico City 06720, 3Laboratory of Immunometabolism, Research Division, General Hospital of Mexico “Dr. Eduardo Liceaga”, Mexico City 06720, 4PECEM, Facultad de Medicina, Universidad Nacional Autónoma de México, Coyoacán, Mexico City 04510, 5Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Plantel Del Valle, Benito Juárez, Mexico City 03100, 6Facultad de Ciencias de la Salud, Universidad Anáhuac, Campus Norte, Huixquilucan, Estado de Mexico 52786, Mexico
Correspondence to: *To whom correspondence should be addressed.
Galileo Escobedo, TEL: 55-2789-2000, FAX: 55-5623-2669
e-mail: gescobedog@msn.com
Lucía A. Méndez-García, TEL: 55-2789-2000, FAX: 55-5623-2669
e-mail: angelica.mendez.86@hotmail.com
†These authors equally contributed to this work.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
The coronavirus family has tropism for the Central Nervous System (CNS), however, there is no solid evidence demonstrating that the neurological effects of COVID-19 result from direct viral infection or systemic inflammation. The goals of this study were to examine the cytokine profile and the presence of SARS-CoV-2 messenger ribonucleic acid (mRNA) in cerebrospinal fluids (CSF) from two patients with cerebrovascular disease and COVID-19. Although the SARS-CoV-2 mRNA was not detected in CSF of both patients, we found abnormally high levels of numerous proinflammatory cytokines and chemokines, especially IL-8 and MCP-1. Since these chemokines mediate activation and recruitment of neutrophils, monocytes, and macrophages, it is feasible that cerebrovascular disease related-neuroinflammation found in both patients results from an exacerbated inflammatory response instead of SARS-CoV-2 direct invasion to CNS. These results suggest that neuroinflammation plays a key role in cerebrovascular disease and COVID-19.
Keywords: SARS-CoV-2, COVID-19, Cerebrospinal fluid, Cerebrovascular disease, IL-8, MCP-1