IgA nephropathy (IgAN) is recognized as most frequent form of primary glomerulonephritis worldwide. IgAN is associated with renal degradation occurring due to irreversible pathological changes leading to glomerulosclerosis and interstitial fibrosis. It remains poorly understood whether and to what extent these changes are followed by the activation of regenerative mechanisms. Therefore, in this study we aimed to evaluate regenerative potential of IgAN patients by quantitating the frequencies of several stem cell types, namely circulating very small embryonic-like stem cells (VSELs), hematopoietic stem cells (HSCs), endothelial progenitor cells (EPCs) as well as different monocyte subsets with varying maturation and angiopoietic potential. Moreover, we analyzed whether changes in stem cell and monocyte frequencies were related to alterations of several chemotactic factors (stromal derived-factor (SDF-1), angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2)) and a marker of monocyte/macrophage activation, namely soluble form of CD163 receptor (sCD163). We showed that IgAN patients presented with enhanced levels of VSELs, but not other stem cell types. We also demonstrated significantly elevated numbers of intermediate monocytes known for their M2-like properties as well as high angiopoietic potential and CD163 expression. This finding was accompanied by detection of elevated sCD163 plasma levels in IgAN patients. Taking together, we demonstrated here that IgAN is associated with selective mobilization of VSELs and increased maturation of monocytes towards M2-like and angiopoietic phenotype. These findings contribute to better understanding of the role of regenerative mechanisms in the pathogenesis of chronic inflammation in the course of IgAN.

Mesenchymal stem cells (MSCs) have a great regenerative and immunomodulatory potential that was successfully tested in numerous pre-clinical and clinical studies of various degenerative, hematological and inflammatory disorders. Over the last few decades, substantial immunoregulatory effects of MSC treatment were widely observed in different experimental models of asthma. Therefore, it is tempting to speculate that stem cell-based treatment could become an attractive means to better suppress asthmatic airway inflammation, especially in subjects resistant to currently available anti-inflammatory therapies. In this review, we discuss mechanisms accounting for potent immunosuppressive properties of MSCs and the rationale for their use in asthma. We describe in detail an intriguing interplay between MSCs and other crucial players in the immune system as well as lung microenvironment. Finally, we reveal the potential of MSCs in maintaining airway epithelial integrity and alleviating lung remodeling. Graphical abstract

The aim of the study was to evaluate the effect of bisphenol A (BPA) on nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression by neutrophils with regard to sex and nuclear factor-κB (NF-κB) pathway participation in this process. This study demonstrated that BPA intensifies the production of NO and the expression of iNOS in the cytoplasmic fraction of neutrophils of women as well as men. In addition, an enhanced expression of NF-κB in the cytoplasmic and nuclear fraction of neutrophils exposed to BPA was observed in the cells of both sexes. The lipopolysaccharide (LPS) stimulation of neutrophils of both sexes led to an intensification of NO production and expression of all tested proteins. However, simultaneous stimulation of neutrophils of both men and women with LPS and BPA decreased the production of NO and expression of iNOS and NF-κB in both fractions compared to the cells exposed only to xenoestrogen. Moreover, expression of iNOS and NF-κB was higher in female neutrophils than in male cells. This study demonstrated that BPA affects the production of NO with the participation of iNOS by human polymorphonuclear neutrophils. This process is associated with the activation of the NF-κB pathway. In addition, different activity of NF-κB in neutrophils, observed with respect to sex, indicates a different role of this pathway in female and male cells.

Lung cancer represents the most common type of human malignancy and is the main cause of cancer-associated mortality worldwide. To improve the effectiveness of treatment strategies, a better understanding of the mechanisms of cancer progression and invasiveness is required. Recently, B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL), two relatively newly described cytokines belonging to the tumor necrosis factor superfamily, have been shown to play a role in cancer progression. However, at present, the effects of both cytokines on lung cancer cells remain unclear. The present study aimed therefore to understand the direct effects of BAFF and APRIL on non-small cell lung cancer (NSCLC) progression. To do so, reverse transcription quantitative PCR and western blotting were used to evaluate whether A549 and H2030 NSCLC cells express receptors for both BAFF and APRIL. The results demonstrated that both investigated cell lines expressed BAFF-R (receptor specific to BAFF only) and transmembrane activator and CAML interactor (TACI; shared receptor for both cytokines). In addition, functional experiments were performed to determine the effects of BAFF and APRIL stimulation on cancer cell viability. The results demonstrated no direct effects of BAFF and APRIL on NSCLC cell proliferation and invasiveness. In summary, the present study demonstrated that NSCLC cells possess the ability to respond directly to both BAFF and APRIL. However, activation of BAFF-R and TACI signaling in cancer cells did not increase the proliferative capacity and invasiveness. Further investigation is thus required to better understand the role of BAFF and APRIL on the progression of NSCLC.

Background: The exact role of individual inflammatory factor in heart failure with reduced ejection fraction (HFrEF) remains elusive. The study aimed to evaluate three monocyte subsets (classical-CD14++CD16−, intermediate-CD14++CD16+, and nonclassical-CD14+CD16++) in HFrEF patients and to assess the effect of the cardiac resynchronization therapy (CRT) on the changes in monocyte compartment. Methods: The study included 85 patients with stable HFrEF. Twenty-five of them underwent CRT device implantation with subsequent 6-month assessment. The control group consisted of 23 volunteers without HFrEF. Results: The analysis revealed that frequencies of non-classical-CD14+CD16++ monocytes were lower in HFrEF patients compared to the control group (6.98 IQR: 4.95–8.65 vs. 8.37 IQR: 6.47–9.94; p = 0.021), while CD14++CD16+ and CD14++CD16− did not differ. The analysis effect of CRT on the frequency of analysed monocyte subsets 6 months after CRT device implantation showed a significant increase in CD14+CD16++ (from 7 IQR: 4.5–8.4 to 7.9 IQR: 6.5–9.5; p = 0.042) and CD14++CD16+ (from 5.1 IQR: 3.7–6.5 to 6.8 IQR: 5.4–7.4; p = 0.017) monocytes, while the frequency of steady-state CD14++CD16− monocytes was decreased (from 81.4 IQR: 78–86.2 to 78.2 IQR: 76.1–81.7; p = 0.003). Conclusions: HFrEF patients present altered monocyte composition. CRT-related changes in the monocyte compartment achieve levels observed in controls without HFrEF.