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

Circulating Ageing Neutrophils as a Marker of Asymptomatic Polyvascular Atherosclerosis in Statin-Naïve Patients without Established Cardiovascular Disease

Background: Current data on the possible involvement of aging neutrophils in atherogenesis are limited. This study aimed to research the diagnostic value of aging neutrophils in their relation to subclinical atherosclerosis in statin-naïve patients without established atherosclerotic cardiovascular diseases (ASCVD). Methods: The study was carried out on 151 statin-naïve patients aged 40–64 years old without ASCVD. All patients underwent duplex scanning of the carotid arteries, lower limb arteries and abdominal aorta. Phenotyping and differentiation of neutrophil subpopulations were performed through flow cytometry (Navios 6/2, Beckman Coulter, USA). Results: The number of CD62LloCXCR4hi-neutrophils is known to be significantly higher in patients with subclinical atherosclerosis compared with patients without atherosclerosis (p = 0.006). An increase in the number of CD62LloCXCR4hi-neutrophils above cut-off values makes it possible to predict atherosclerosis in at least one vascular bed with sensitivity of 35.4–50.5% and specificity of 80.0–92.1%, in two vascular beds with sensitivity of 44.7–84.4% and specificity of 80.8–33.3%. Conclusion: In statin-naïve patients 40–64 years old without established ASCVD with subclinical atherosclerosis, there is an increase in circulating CD62LloCXCR4hi-neutrophils. It was also concluded that the increase in the number of circulating CD62LloCXCR4hi-neutrophils demonstrated moderate diagnostic efficiency (AUC 0.617–0.656) in relation to the detection of subclinical atherosclerosis, including polyvascular atherosclerosis

Synthesis, Structure and Photoluminescence Properties of Cd and Cd-Ln Pentafluorobenzoates with 2,2′:6′,2′-Terpyridine Derivatives

Six new complexes [Cd(tpy)(pfb)2] (1, tpy = 2,2′:6′,2″-terpyridine), [Ln2Cd2(tpy)2(pfb)10] (Ln = Eu (2Eu), Tb (2Tb)), [Ln2Cd2(tbtpy)2(pfb)10]·2MeCN (Ln = Eu (3Eu), Tb (3Tb), tbtpy = 4,4′,4″-tri-tert-butyl-2,2′:6′,2″-terpyridine), [Eu2Cd2(tppz)(pfb)10]n (4, tppz = 2,3,5,6-tetra-(pyridin-2-yl)pyrazine) based on pentafluorobenzoic acid (Hpfb) have been prepared and investigated. The effect of tridentate ligands on geometry heterometallic scaffolds synthesized complexes is discussed. The supramolecular crystal structures of the new compounds are stabilized by π-π, C-F···π, C-H···O, C-H...F, F….F interactions. Non-covalent interactions have been studied using Hirschfeld surface analysis. The obtained compounds were characterized by single-crystal and powder X-ray diffraction, luminescence spectroscopy, IR spectroscopy, CHN analysis. Complexes 2Ln and 3Ln exhibit metal-centered photoluminescence, but the presence of ligand luminescence bands indicates incomplete energy transfer from the d-block to the lanthanide ion