Objective To summarize the bioactive substances contained in bacterial extracellular vesicles (EVs) and their mechanisms in mediating bacterial-bacterial and bacterial-host interactions, as well as their mechanisms for use in implant infection-associated clinical guidance. Methods A wide range of publications on bacterial-derived EVs were extensively reviewed, analyzed, and summarized. Results Both gram-negative bacteria (G– bacteria) and gram-positive bacteria (G+ bacteria) can secrete EVs which contain a variety of bioactive substances, including proteins, lipids, nucleic acids, and virulence factors, and mediate bacterial-bacterial and bacterial-host interactions. EVs play an important role in the pathogenic mechanism of bacteria. Conclusion Bioactive substances contained within bacteria-derived EVs play an important role in the pathogenesis of bacterial infectious diseases. In-depth study and understanding of their pathogenic mechanisms can provide new insights which will improve early clinical diagnosis, prevention, and treatment of implant-associated infection. However, at present, research in this area is still in its infancy, and many more in-depth mechanisms need to be further studied.
Seawater drowning leads to acute lung tissue structure injury, lung ventilation and air exchange dysfunction, acute pulmonary edema, and even acute respiratory failure. The pathogenesis of seawater induced acute lung injury is complex, involving inflammatory response, pulmonary edema, pulmonary surfactant, oxidative stress, apoptosis and autophagy. Timely and effective treatment is the key to reduce the mortality and disability rate of patients with seawater induced acute lung injury. This article summarizes the research progress in the pathogenic mechanism and treatment strategy of seawater induced acute lung injury, aiming to provide reference for the comprehensive treatment of seawater induced acute lung injury patients in clinical work and subsequent related research.
Most immune-related adverse event (irAE) associated with immune checkpoint inhibitors (ICIs) resulted from excessive immune response against normal organs. The severity, timing, and organs affected by these events were often unpredictable. Adverse reactions could cause treatment delays or interruptions, in rare cases, pose a life-threatening risk. The mechanisms underlying irAE involved immune cell dysregulation, imbalances in inflammatory factor expression, alterations in autoantibodies and complement activation, even dysbiosis of intestinal microorganisms. However, the mechanisms of irAE occurrence might differ slightly among organs due to variations in their structures and the functions of resident immune cells. Future research should focus on the development of targeted drugs for the prevention or treatment of irAE based on the mechanisms by which irAE occurs in different organs. A deeper understanding of the mechanisms underlying irAE occurrence would aid clinicians in effectively utilizing ICIs and provide valuable guidance for their clinical application.