Role of inflammation in the pathogenesis of novel coronavirus infection

Abstract

The activation of various types of epithelial, endothelial, and immunocompetent cells, along with hyperproduction of cytokines and other proinflammatory mediators and activation of the complement system, plays a crucial in the pathogenesis of coronavirus disease 2019 (COVID-19). These conditions leads to severe inflammation and acute respiratory distress syndrome. Hyperinflammatory reactions in the lungs and other tissues result in significant tissue damage and organ dysfunction. A specific feature of severe acute respiratory syndrome coronavirus 2 infection is the combination of cell death and inflammation. In COVID-19, not only pneumocytes but also many other cells are killed. These cells undergo programed cell death through three main pathways: apoptosis, pyroptosis, and necroptosis. These processes help protect organisms from intracellular pathogens by releasing them from infected cells, which then bind to specific receptors and antibodies, undergo opsonization, and are phagocytosed. Localized inflammation aims to eliminate these pathogens, but severe inflammation is an important component of the immunopathogenesis of COVID-19. The immunopathogenesis of COVID-19, particularly the role of inflammation in the development of severe clinical signs, is now largely understood. This disease has a complex immunopathology, including excessive activation of adaptive and innate branches of the immune system and interactions between immune cells and affected tissues.