The present review highlights the complex interactions between cancer and neutrophil extracellular traps (NETs). Neutrophils constitute the first line of defense against foreign invaders using major effector mechanisms: phagocytosis, degranulation, and NETs formation. NETs are composed from decondensed nuclear or mitochondrial DNA decorated with proteases and various inflammatory mediators. Although NETs play a crucial role in defense against systemic infections, they also participate in non-infectious conditions, such as inflammation, autoimmune disorders, and cancer. Cancer cells recruit neutrophils (tumor-associated neutrophils, TANs), releasing NETs to the tumor microenvironment. NETs were found in various samples of human and animal tumors, such as pancreatic, breast, liver, and gastric cancers and around metastatic tumors. The role of the NETs in tumor development increasingly includes cancer immunoediting and interactions between the immune system and cancer cells. According to the accumulated evidence, NETs awake dormant cancer cells, causing tumor relapse, as well as its unconstrained growth and spread. NETs play a key regulatory role in the tumor microenvironment, such as the development of distant metastases through the secretion of proteases, i.e., matrix metalloproteinases and proinflammatory cytokines. NETs, furthermore, directly exacerbate tumor aggressiveness by enhancing cancer migration and invasion capacity. The collected evidence also states that through the induction of the high-mobility group box 1, NETs induce the epithelial to mesenchymal transition in tumor cells and, thereby, potentiate their invasiveness. NET proteinases can also degrade the extracellular matrix, promoting cancer cell extravasation. Moreover, NETs can entrap circulating cancer cells and, in that way, facilitate metastasis. NETs directly trigger tumor cell proliferation through their proteases or activating signals. This review focused on the pro-tumorigenic action of NETs, in spite of its potential to also exhibit an antitumor effect. NET components, such as myeloperoxidase or histones, have been shown to directly kill cancer cells. A better understanding of the crosstalk between cancer and NETs can help to devise novel approaches to the therapeutic interventions that block cancer evasion mechanisms and prevent metastatic spread. This review sought to provide the most recent knowledge on the crosstalk between NETs and cancer, and bring more profound ideas for future scientists exploring this field.

Sepsis is an overwhelming inflammatory response to infection, resulting in multiple-organ injury. Neutrophils are crucial immune cells involved in innate response to pathogens and their migration and effector functions, such as phagocytosis and neutrophil extracellular trap (NET) formation, are dependent on cytokine presence and their concentration. In the course of sepsis, recruitment and migration of neutrophils to infectious foci gradually becomes impaired, thus leading to loss of a crucial arm of the innate immune response to infection. Our review briefly describes the sepsis course, the importance of neutrophils during sepsis, and explains dependence between cytokines and their activation. Moreover, we, for the first time, summarize the impact of cytokines on phagocytosis and NET formation. We highlight and discuss the importance of cytokines in modulation of both processes and emphasize the direction of further investigations.

Acute leukemias, the most common cancers in children, are characterized by excessive proliferation of malignant progenitor cells. As a consequence of impaired blood cell production, leukemia patients are susceptible to infectious complications—a major cause of non-relapse mortality. Neutrophil extracellular traps (NETs) are involved in various pathologies, from autoimmunity to cancer. Although aberrant NETs formation may be partially responsible for immune defects observed in acute leukemia, still little is known on the NET release in the course of leukemia. Here, we present the first comprehensive evaluation of NETs formation by neutrophils isolated from children with acute leukemia in different stages of the disease and treatment stimulated in vitro with phorbol 12-myristate 13-acetate (PMA), N-formyl-methionyl-leucyl-phenylalanine (fMLP), and calcium ionophore (CI). NETs release was measured using quantitative fluorescent method and visualized microscopically. In this setting, NETs release was significantly impaired in leukemic children both at the diagnosis and during the treatment, and full restoration of neutrophil function was achieved only after successful completion of the leukemia treatment. We suggest that neutrophil function impairment may result from both disease- and treatment-related factors. In this context, deficient innate immune response observed in acute leukemia patients may be present regardless of neutrophil count and contribute to secondary immunodeficiency observed in this population.

Objective The objective of this study was to assess the emerging biochemical markers of arterial remodeling in patients with morbid obesity before and after surgical treatment and to compare the results to a control group. Material and Methods The prospective study included 40 patients with BMI 47.73 ± 6.18 kg/m², qualified for elective bariatric surgery and re-examined 6 months after the surgery. The control group consisted of non obese, age and sex matched 15 subjects. Following laboratory examinations were performed in all patients: basic laboratory examinations, MMP-2, MMP-9, adiponectin, PAI-1, CD40L, E-selectin. Results Examination of patients 6 m after bariatric surgery revealed a 34.57 ± 9.71 reduction in excess body weight. Comparison of the study group at two time points revealed differences in adiponectin, MMP-2 and MMP-9 levels. Hypoadiponectinemia was observed in 35 % patients 6 months after bariatric surgery compared to 90 % patients before the surgery. In addition, a strong correlation was observed between body fat mass and adiponectin levels (r = −0.504, p = 0.055). Moderate correlations were demonstrated between E-selectin levels and BMI (r = 0.361; p = 0.022), and metalloproteinase-9 levels (r = 0.326; p = 0.040). In addition, strong relationship was demonstrated between MMP-2 and MMP-9 (r = 0.502; p = 0.001), and moderate between MMP-2 and adiponectin levels (r = 0.449; p = 0.003). MMP-9 levels were moderately correlated with HDL-cholesterol levels (r = 0.316; p = 0.046). Conclusions Assessment of laboratory markers of arterial remodeling and metabolism suggest their adverse changes in patients with morbid obesity. However, body mass reduction due to bariatric surgery decreases inflammatory status, improves biochemical markers of arterial remodeling as well as to beneficial changes in the metabolism.

An improved understanding of the vascular function, measured in non-invasive way, in constantly growing group of patients at increased risk of cardiovascular events is necessary. To evaluate the effects of metabolic syndrome in morbidly obese patients and body mass reduction secondary to gastric bypass surgery on convenient and new non-invasive markers of artery function: pulse wave velocity (PWV), flow- and nitroglycerin-mediated dilatation (FMD, NTG). There were 40 patients included into prospective study, who were qualified for bariatric surgery (OB1) and evaluated again 6 m after surgery (OB2). A control group (CG) consisted of 15 healthy women. A second control group (CG2) consisted of 15 women with grade 1 obesity. PWV, FMD, NTG were assessed. The reduction of BMI (kg/m2) from 47.73 ± 6.18 (OB1) to 35.22 ± 5.20 (OB2) was observed. The PWV turned out to be higher before bariatric surgery (OB1 vs. OB2 8.53 ± 1.76 vs. 7.82 ± 1.49 m/s; p < 0.001), however it was no different than PWV in CG. In OB1 group PWV showed correlation with age (r = 0.492, p = 0.001), HR (r = 0.324, p = 0.04), %FM (r = 0.328; p = 0.039), NTG% (r = −0.332, p = 0.036) as well as hsCRP (r = 0.394, p = 0.014). A multivariate analysis showed that the most significant factors influencing PWV were age (p = 0.0005) and hsCRP (p = 0.0014), pseudo R2 index 0.44365. The values of FMD differed between OB1 and OB2 groups (12.83 ± 5.15 vs. 17.52 ± 5.50 %; p < 0.0001), however, they were similar to results obtained in CG (14.45 ± 6.14 %; NS). The values of nitroglycerin-mediated dilatation differed between OB1 and OB2 groups (21.47 ± 8.31 vs. 28.54 ± 8.16 %; p < 0.0001) and were lower as compared with CG (31.42 ± 5.95 %; p = 0.0005). Body mass reduction secondary to bariatric surgery in patients with severe obesity and metabolic syndrome results in improvement of functional markers of artery function and advantageous metabolic changes. The improvement in functional markers of artery function (NTG%) was correlated with change in triglyceride blood concentration.

Currently, extracellular vesicles (EVs) have been implicated in the etiopathogenesis of many diseases, including lung disorders, with the possibility of diagnostic and therapeutic applications. The analysis of EV in respiratory tract diseases faces many obstacles, including material collection from airways, standardization of isolation techniques, detection methods, the analysis of their content, etc. This review focuses on the role of extracellular vesicles in the pathogenesis of atopic respiratory diseases, especially asthma, with a special focus on their clinical applicability as a diagnostic tool. We also summarize available laboratory techniques that enable the detection of EVs in various biological materials, with particular emphasis on flow cytometry. The opportunities and limitations of detecting EV in bronchoalveolar lavage fluid (BALF) were also described.