Abstract
Anesthetics have immunomodulatory effects, but the use of different assay systems has contributed to inconsistent results in the literature. IL-1β and reactive oxygen species (ROS) secreted by phagocytes are important factors that protect against Staphylococcus aureus infection. In this study, the effects of four intravenous anesthetics (propofol, thiamylal sodium, midazolam, and ketamine) on IL-1β secretion, ROS, and bacterial survival in S. aureus-infected RAW264.7 cells were evaluated. S. aureus-infected RAW264.7 cells with or without intravenous anesthetic treatment were established as the experimental model. Cell supernatants were subjected to ELISAs to measure secreted IL-1β. Cell pellets were subjected to qPCR and western blot analyses to analyze IL-1β mRNA and protein levels. Luminol chemiluminescence assays were used to detect ROS, and bacterial survival was determined by counting the colony forming units at the beginning and end of the infection. Compared with the levels after treatment with the other intravenous anesthetics, secreted IL-1β levels were lowest in the supernatant of S. aureus-infected RAW264.7 cell cultures after propofol treatment, but propofol did not decrease IL-1β mRNA or protein expression. However, thiamylal sodium and midazolam decreased IL-1β mRNA and protein expression in a dose-dependent manner. Additionally, propofol substantially decreased S. aureus-stimulated ROS and phagocytosis. Bacterial survival was strongly increased by propofol treatment. Of the four intravenous anesthetics, propofol was the most potent inhibitor of IL-1β secretion and ROS level in S. aureus-infected RAW264.7 cells; moreover, propofol resulted in an increase in bacterial survival by inhibiting ROS and phagocytosis.
Highlights
Intravenous anesthetics may be used for the sedation of perioperative and critically ill patients and have potential immunomodulatory effects [1,2,3]
We further examined whether propofol promoted bacterial survival by minimizing the phagocytic ability and found that propofol inhibited the phagocytosis of S. aureus BioParticles (Fig. 5a)
We used a model of S. aureus-infected RAW264.7 cells and found that of four intravenous anesthetics, propofol was the most effective agent for inhibiting IL-1β secretion, but this anesthetic did not decrease IL-1β mRNA or pro-IL-1β biosynthesis
Summary
Intravenous anesthetics may be used for the sedation of perioperative and critically ill patients and have potential immunomodulatory effects [1,2,3]. Intravenous anesthetics can inhibit human phagocyte functions, including chemotaxis, cytokine secretion, phagocytosis, and reactive oxygen species (ROS) generation [1, 4,5,6,7,8]. The disruption of any phagocyte function could result in bacterial infections. Staphylococcus aureus is one of the most important pathogens that cause human morbidity and mortality worldwide [9]. S. aureus acts via several mechanisms to escape host immune defenses and establish an infection, including resisting antimicrobial peptides, clearing ROS, inhibiting complement activation and neutrophil recruitment, and evading phagocytosis [12, 13]
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