ABSTRACT
Objective: Pneumonia is an infectious inflammation of the alveoli,distal airway,and interstitium caused by bacterial,viral,and other pathogens. Maxing Shigantang,originated from Treatise On Cold Damage Diseases,is a classic prescription for treating pneumonia,with significant clinical efficacy. However,its treatment mechanism is still elusive. Method(s): In that paper,the transcriptome-based multi-scale network pharmacology was used to reveal the overall pharmacological mechanism of Maxing Shigantang in treating pneumonia from six scales of tissue,cell,pathological process,biological process,signaling pathway, and target. Result(s):At the tissue level,Maxing Shigantang mainly acted on the focal tissue of pneumonia-lung and the main inflammatory immune tissues-blood and spleen. Analysis of cell,pathological process and biological process suggested that Maxing Shigantang could treat pneumonia by reversing inflammatory and immune functions and improving cardiopulmonary and vascular injury caused by pneumonia. Analysis of signaling pathway and target showed that Maxing Shigantang regulated inflammatory immune response pathways such as "coronavirus disease-COVID-19" and "Toll-like receptor signaling pathway",and related targets such as "MAPKAPK3" and "NRG1". Conclusion(s):This paper,from molecular to tissue levels,indicated Maxing Shigantang treated pneumonia mainly by regulating inflammatory immune response and improving cardiopulmonary and vascular injury.Copyright © 2023, China Academy of Chinese Medical Sciences Institute of Chinese Materia Medica. All rights reserved.
ABSTRACT
The role of matrix metalloproteinases (MMPs) in pathogenesis and severity of coronavirus disease 2019 (COVID-19) is under extensive exploration. MMPs are a family of extracellular proteases involved in a variety of physiological and pathological processes and conditions. The role of MMPs in COVID-19 stems from the pathogenesis resulting in the release of chemokines and pro-inflammatory markers which cause pulmonary oedema. In addition, the approaches to treatment of COVID-19 often are associated with some complications like acute lung injury due to extracellular matrix remodelling. In this respect, the aim of this review is to summarize, interpret and evaluate the significance of matrix metalloproteinases in SARS-CoV-2 infection in terms of the severity of the condition and delve into potential treatment from this perspective as well as highlighting the physiological and protective role of some MMPs. © 2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.
ABSTRACT
Infectious diseases continue to represent a major threat to the humankind. This is reiterated by the current COVID-19 pandemic that affected almost 550 million people worldwide and caused more than 6.35 million deaths. It is clear that in addition to the existing preventive measures and treatments for various pathogens, better understanding is needed of the relationship between pathogen infection and the human antiinfection immune response and of the specific mechanisms underlying these complex processes. There is a constant warfare between the hosts and infectious pathogens, where humans have evolved a very effective and broadly amended antiinfection immune system, but, in their turn, pathogens have evolved a multitude of immune escape mechanisms to efficiently oppose it. It is recognized now that liquid–liquid phase separation (LLPS) occupies a special place among the important molecular mechanisms of the antiinfection immune response. Some illustrative examples of the roles of LLPS in the antiinfection immune response are considered in this chapter.
ABSTRACT
The COVID-19 pandemic examines not only the state of actual health care but also the state of fundamental medicine in various countries. Pro-inflammatory processes extend far beyond the classical concepts of inflammation. They manifest themselves in a variety of ways, beginning with extreme physiology, then allostasis at low-grade inflammation, and finally the shockogenic phenomenon of "inflammatory systemic microcirculation". The pathogenetic core of critical situations, including COVID-19, is this phenomenon. Microcirculatory abnormalities, on the other hand, lie at the heart of a specific type of general pathological process known as systemic inflammation (SI). Systemic inflammatory response, cytokine release, cytokine storm, and thrombo-inflammatory syndrome are all terms that refer to different aspects of SI. As a result, the metabolic syndrome model does not adequately reflect the pathophysiology of persistent low-grade systemic inflammation (ChSLGI). Diseases associated with ChSLGI, on the other hand, are risk factors for a severe COVID-19 course. The review examines the role of hypoxia, metabolic dysfunction, scavenger receptors, and pattern-recognition receptors, as well as the processes of the hemophagocytic syndrome, in the systemic alteration and development of SI in COVID-19.