Abstract
The coronavirus disease 2019 (COVID-19) pandemic has claimed over 2.7 million lives globally. Obesity has been associated with increased severity and mortality of COVID-19. However, the molecular mechanisms by which obesity exacerbates COVID-19 pathologies are not well-defined. The levels of free fatty acids (FFAs) are elevated in obese subjects. This study was therefore designed to examine how excess levels of different FFAs may affect the progression of COVID-19. Biological molecules associated with palmitic acid (PA) and COVID-19 were retrieved from QIAGEN Knowledge Base, and Ingenuity Pathway Analysis tools were used to analyze these datasets and explore the potential pathways affected by different FFAs. Our study found that one of the top 10 canonical pathways affected by PA was the coronavirus pathogenesis pathway, mediated by key inflammatory mediators, including PTGS2; cytokines, including IL1β and IL6; chemokines, including CCL2 and CCL5; transcription factors, including NFκB; translation regulators, including EEF1A1; and apoptotic mediators, including BAX. In contrast, n-3 fatty acids may attenuate PA’s activation of the coronavirus pathogenesis pathway by inhibiting the activity of such mediators as IL1β, CCL2, PTGS2, and BAX. Furthermore, PA may modulate the expression of ACE2, the main cell surface receptor for the SARS-CoV-2 spike protein.
Highlights
Among the 35 biological molecules overlapped between palmitic acid (PA)- and COVID-19-associated molecules retrieved from QIAGEN Knowledge Base (QKB), 20 were involved in immune regulation, and some of these molecules, such as EEF1A, IL1β, IFNB1, IL6, C motif chemokine ligand 2 (CCL2), CXCL8, C motif chemokine ligand 5 (CCL5), prostaglandin-endoperoxide synthase 2 (PTGS2), and FOS, were mapped to the paths from PA to the coronavirus pathogenesis pathway
We found that PA may (1) activate the transcription factors, such as FOS and NF-κB, that regulate the expression of inflammatory mediators; (2) increase the activity of molecules contributing to apoptosis, such as EIF2AK3, activating transcription factor 4 (ATF4), CASP8, CASP9, and BAX; (3) enhance the activity of PTGS2; and (4) increase the production of cytokines, including IL1β and IL6, and chemokines, including CCL2, CCL5, and
We found that PA may increase the activities of PTGS2, chemokines, such as CCL5, CCL2, and CXCL8, cytokines, such as IFNB1, IL6, and IL1β, transcription factors, such as FOS; and translation regulators, such as eukaryotic elongation factor 1-alpha 1 (EEF1A1), which, in turn, mildly increases the activity of Angiotensin converting enzyme 2 (ACE2)
Summary
Academic Editors: Atsushi Tanaka and Koichi NodeReceived: 11 May 2021Accepted: 26 June 2021Published: 1 July 2021Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.Licensee MDPI, Basel, Switzerland.Attribution (CC BY) license (https://creativecommons.org/licenses/by/ 4.0/).The coronavirus disease 2019 (COVID-19) is caused by infection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). To date, there have been more than 120 million confirmed COVID-19 cases and more than 2.7 million deaths reported by the World Health Organization (WHO) [1]. While some may be asymptomatic, many
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
