From Innate Immunity to Inflammation: A Primer on Multiple Facets of NF-κB Signaling in COVID-19

Abstract

Nuclear factor-kappa B (NF-κB) induces the expression of many pro-inflammatory genes, including cytokines and chemokines. In the past decades, a wealth of clinical as well as animal model-based studies have demonstrated the association of the deregulated NF-κB signaling pathway with the progression of various inflammatory diseases, including inflammatory bowel disease (IBD), multiple sclerosis (MS), and chronic obstructive pulmonary disease (COPD). Given the conserved role of the NF-κB pathway as the pivotal regulator of pro-inflammatory gene expression, different components of the NF-κB pathway are proposed as major therapeutic targets against these diseases. The ongoing coronavirus disease of 2019 (COVID-19) has posed a significant public health crisis regarding inflammation-related diseases. A robust inflammatory response is associated with COVID-19-infection-related complications, including muti-organ failure and death. This review summarizes the past and current state of knowledge on the role of the NF-κB signaling pathway in the innate immune response and inflammatory diseases with the objective of potential therapeutic use in developing effective treatment options for COVID-19.