Background: Barbiturates and propofol are used for deep sedation of patients with elevated intracranial pressure refractory to standard therapeutic regimens. Such patients often suffer from bacterial infections, which are most commonly caused by Staphylococcus aureus. Various interactions of anesthetics with components of the host defense have been documented, but very little is known about the influence on monocytes, which are a first-line defense against bacterial invasion. Therefore, we studied the effects of thiopental, methohexital, and propofol on monocyte phagocytosis using an in vitro whole blood model of viable S. aureus.
Materials And Methods: Whole blood samples were preincubated with different concentrations of thiopental, methohexital, and propofol. Phagocytosis was stopped at different time points after addition of viable S. aureus. Monocytes then were stained with monoclonal antibodies for flow cytometric analysis of monocyte recruitment (ratio of ingesting monocytes). Furthermore, the fluorescence intensity of ingested bacteria served as semiquantitative measurement of phagocytosis activity.
Results: Both barbiturates inhibited monocyte recruitment and phagocytosis activity concentration-dependently, whereas propofol did not affect any of the investigated parameters. At concentrations of 7.6 x10(-3) M thiopental or 1.1 x 10(-3) M methohexital and greater, monocyte recruitment and phagocytosis activity were significantly inhibited. The calculated half-maximum inhibitory concentration (IC50) of thiopental was 8.4 x 10(-3) M for monocyte recruitment and 8.6 x 10(-3) M for phagocytosis activity. The corresponding values for methohexital were 4.1 x 10(-3) M and 1.1 x 10(-3) M, respectively.
Conclusion: The two barbiturates induce concentration-dependent inhibition of monocyte phagocytosis, whereas propofol is without effect. In combination with previously described effects on granulocyte function, these findings suggest that defense against bacterial infection might be reduced by barbiturates.
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http://dx.doi.org/10.1007/s15010-007-7240-3 | DOI Listing |
Clin Immunol
December 2024
Univ Rennes, INSERM, EHESP, IRSET (Institut de recherche en santé, environnement et travail) - UMR_S 1085, F-35000 Rennes, France. Electronic address:
Occupational exposure to crystalline silica is etiologically linked to an increased incidence of systemic sclerosis (SSc), also called Erasmus syndrome. The underlying mechanisms of silica-related SSc are still poorly understood. We demonstrated that early and repeated silica exposure contribute to the severity of SSc symptoms in the hypochloric acid (HOCl)-induced SSc mouse model.
View Article and Find Full Text PDFOpen Med (Wars)
December 2024
Shandong University of Traditional Chinese Medicine, Jinan, 250014, China.
Background: Atherosclerosis is a lipid-driven inflammatory disease characterized by plaque formation in major arteries. These plaques contain lipid-rich macrophages that accumulate through monocyte recruitment, local macrophage differentiation, and proliferation.
Objective: We identify the macrophage subsets that are closely related to atherosclerosis and reveal the key pathways in the progression of atherosclerotic disease.
J Inflamm Res
December 2024
National Metabolic Management Center, Longyan First Affiliated Hospital of Fujian Medical University, Longyan, Fujian, 364000, People's Republic of China.
Background: Emerging evidence suggests that increased perirenal adipose tissue (PAT) may trigger systemic inflammation and oxidative stress, potentially contributing to hyperuricemia (HUA). This study aimed to explore the link between PAT and HUA risk, and the potential mediating role of inflammation and oxidative stress.
Methods: This study recruited 903 participants with T2DM.
Front Med (Lausanne)
December 2024
Metabolismo Óseo, Vascular y Enfermedades Inflamatorias Crónicas, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Oviedo, Spain.
Introduction: Cardiovascular disease is the major cause of premature death in chronic kidney disease (CKD) and vascular damage is often detected belatedly, usually evaluated by expensive and invasive techniques. CKD involves specific risk factors that lead to vascular calcification and atherosclerosis, where inflammation plays a critical role. However, there are few inflammation-related markers to predict vascular damage in CKD.
View Article and Find Full Text PDFAdv Sci (Weinh)
December 2024
Guangdong Provincial Clinical Research Center for Orthopedic Diseases, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Staphylococcus aureus (S. aureus) is a leading cause of Periprosthetic joint infection (PJI), a severe complication after joint arthroplasty. Immunosuppression is a major factor contributing to the infection chronicity of S.
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