Abstract
Equilibrium within the immune system can often determine the fate of its host. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the pathogen responsible for the coronavirus disease 2019 (COVID-19) pandemic. Immune dysregulation remains one of the main pathophysiological components of SARS-CoV-2-associated organ injury, with over-activation of the innate immune system, and induced apoptosis of adaptive immune cells. Here, we provide an overview of the innate immune system, both in general and relating to COVID-19. We specifically discuss “NETosis,” the process of neutrophil release of their extracellular traps, which may be a more recently described form of cell death that is different from apoptosis, and how this may propagate organ dysfunction in COVID-19. We complete this review by discussing Stem Cell Therapies in COVID-19 and emerging COVID-19 phenotypes, which may allow for more targeted therapy in the future. Finally, we consider the array of potential therapeutic targets in COVID-19, and associated therapeutics.
Highlights
Equilibrium within the immune system can often determine the fate of its host
Subsequent viral RNAs serve as pathogenassociated molecular patterns (PAMPs), which are sensed by Toll-like receptors (TLRs) [2]
They are activated through PAMPs or self-derived damage-associated molecular patterns (DAMPs) binding to pathogen recognition receptors (PRRs) like TLRs, NODlike receptors (NLR), and RIG-I-like helicases
Summary
Equilibrium within the immune system can often determine the fate of its host. In sepsis, and many other inflammatory syndromes, the host’s immune system performs a balancing act between the protection it offers through eradication of the offending pathogen, vs. the constant threat of an immune-mediated pathophysiological maelstrom. Subsequent viral RNAs serve as pathogenassociated molecular patterns (PAMPs), which are sensed by Toll-like receptors (TLRs) [2] This results in epithelial cell activation, initiating a cascade of innate immune cell chemoattraction (Figure 1) [3]. This immune cell infiltration causes acute respiratory distress syndrome (ARDS) locally in the lungs, and septic shock, coagulation dysfunction, and multiple organ dysfunction syndrome beyond the lungs [2]. The mechanisms behind this distal organ injury are multiple, but immune dysregulation remains one of the main pathophysiological aetiologies. This review will focus on the innate immune system in COVID-19-induced sepsis and subsequently discusses stem cell therapies, emerging COVID-19 phenotypes and potential therapeutic targets
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