病原始动刺激分子集合/分子对：脓毒症病原学研究的新视角及其应用

Sepsis is a systemic acute and severe condition caused by pathogen infection, which poses a life-threatening risk due to its involvement or accompanying consequence of multiorgan failure. During the COVID-19 pandemic, sepsis was one of the key mechanisms leading to death in COVID-19 patients. Currently, however, there is a lack of systematic comparison regarding the similarities and differences between the mechanisms by which a common pathogen causes host tissue/organ damages and those that lead to sepsis. Most studies have been limited to the interactions between pathogen-associated molecular patterns (PAMPs) and pattern recognition receptors (PRRs). COVID-19-related sepsis clearly indicates that the molecular pathways through which SARS-CoV-2 initiates disease and ultimately causes sepsis are primarily via the binding of its spike proteins to the host cell′s ACE2 receptors, rather than through PAMPs (such as viral RNA) stimulating PRRs/TLR7. Integrating other evidence regarding pathogen-host interactions (e.g. Pseudomonas aeruginosa flagellar hook protein FlgE stimulating ectopic ATP synthase on surface of vascular endothelial cells), this paper proposes that all molecules of a specific pathogen capable of eliciting reactions in host components constitute the "pathogen-initiated stimulatory molecular panel" (PSMPL), which represents the inherent and relatively constant biological characteristics of that pathogen. Furthermore, all molecular-molecular pairings formed by PSMPL within the host constitute the starting points of all interaction pathways between the pathogen and the host, referred to as "pathogen-initiated stimulatory molecular pairs" (PSMPS). The combinational effects of these molecular pair-mediated stimulations determine the net impact of the pathogen on host cells, tissues, or organs. The introduction of the PSMPL and PSMPS concepts will facilitate deeper and more comprehensive studies of pathogen-host interactions, help to identify new pathways and mechanisms leading to sepsis, and promote the discovery of novel therapeutic targets for sepsis.