Neutrophil extracellular traps in the fight against biofilm-forming microorganisms: hunters or prey?

The review presents up-to-date data on the relationships between neutrophil extracellular traps (NETs) and biofilm-forming microorganisms P aeruginosa, S. aureus, Candida spp. obtained in vitro and in vivo studies. Up to 80% of human microbial infections are associated with biofilm-forming microorganisms. The formation of highly specialized biofilm communities is one of the main strategies for the survival of bacteria and fungi, significantly increasing their tolerance to aggressive and stressful environmental conditions, chemotherapeutic drugs, and immune system factors, contributing to their persistence and chronicity of the infectious process. The formation of NETs in the process of NETosis is one of the biological mechanisms used by neutrophils in protection against pathogens. Chemoattractants of biofilm origin, as well as those secreted by epithelial and immunocompetent cells, attract and activate migrating neutrophils. However, given that bacteria form fairly large cell clusters and aggregates in biofilms, the process of phagocytosis is sometimes difficult or impossible. Under these conditions, it is logical to assume that the importance of NETs in anti-biofilm immunity increases. However, due to the components of the extracellular biofilm matrix (e.g., Psl exopolysaccharide P aeruginosa), quorum sensing (QS) molecules (e.g., LasR QS system P aeruginosa), enzymes (e.g., LasA protease and LasB elastase P. aeruginosa), toxins (e.g., Panton-Valentine leukocidin and AB Y-hemolysin S. aureus) and probably other factors yet to be studied, the microorganisms in biofilms are able to influence the signaling systems involved in NETosis, the intensity of the formation of NETs, the sequestration and killing mechanisms in them, sometimes subordinating and using NETs components for their own purposes

Intensity of CD36 expression by monocyte subpopulations and blood lipid spectrum parameters in patients without established atherosclerotic cardiovascular disease

Introduction. At the current stage of the study of atherosclerosis, it has been established that chronic activation of innate immunity, causing persistent low-intensity sterile inflammation, plays a crucial role at all stages of atherogenesis. Laboratory evaluation of signaling pathways associated with molecular patterns (DAMPs) in atherosclerosis and related to cardiovascular diseases (CVD) may contribute to the discovery of new diagnostic and prognostic markers. Objective: to study the relationship between lipid metabolism parameters and CD36 exposure to circulating monocytes in patients without established CVD. Material and methods. The study included 42 patients aged 4064 years without established atherosclerotic CVD, 19 (45.2 %) men and 23 (54.7 %) women. Dyslipidemia was detected in 95.2 % of patients. The blood serum concentrations of total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides, glucose, glycated hemoglobin, high-sensitivity C-reactive protein (hs-CRP), creatinine were determined with subsequent calculation of glomerular filtration rate. Phenotyping of circulating monocyte subpopulations was performed by flow cytometry on a Navios 6/2 device (Beckman Coulter, USA). Results and discussion. According to the results of correlation analysis, non-HDL cholesterol levels were inversely correlated with absolute (r = 0.394; p = 0.013) and relative (r = 0.432; p = 0.006) content of CD14+CD16++CD36+TLR2+ monocytes. LDL cholesterol levels were also inversely correlated with the relative content of CD14+CD16+CD36+TLR2+ monocytes (r = 0.417; p = 0.018). According to correlation analysis, the level of non-HDL cholesterol inversely correlated with the intensity of CD36 expression on classical (r = -0.650; p < 0.0001), intermediate (r = 0.323; p = 0.045) and non-classical (r = 0.480; p = 0.002) monocytes. Also, CD36 expression intensity on classical (r = 0.449; p = 0.004) and non-classical (r = 0.382; p = 0.016) monocytes was inversely correlated with remnant cholesterol levels. In addition, increased non-HLA cholesterol levels were associated with decreased TLR2 expression on CD14+ CD16++ monocytes (r = 0.381; p = 0.018). It should be noted that a decrease in CD36 expression on intermediate monocytes was also associated with an increase in hs-CRP (r = 0.657; p = 0.003). Conclusion. In patients without established atherosclerotic CVD, an increase in cholesterol content of atherogenic lipoprotein fractions was associated with a decrease in the number of CD14+CD16++ and CD14+CD16+ monocytes co-expressing CD36 and TLR2 as well as with a decrease in CD36 expression on classical, intermediate and non-classical monocytes