Background and Objectives: One of the members of the neurotrophin (NT) family is the brain-derived neurotrophic factor (BDNF). In addition to its role in the nerve system, it has been found to play a role in lung health and diseases. Materials and Methods: The serum concentrations of BDNF were assessed in 57 patients with COPD and in 19 control individuals and the possible associations of BDNF with the spirometric indexes and disease stages were explored. Results: We did not find a significant difference between the serum concentrations of BDNF of patients and controls (p = 0.521). A significant negative correlation of the serum BDNF levels with the age of the patients (Rho = −0.279, p = 0.036) was observed. In addition, a borderline negative correlation with the age of disease onset (Rho= −0.244, p = 0.063) was also found. When analyzing these correlations in different genders, we found stronger statistical significance in male patients (Rho = −0.398, p = 0.009; and Rho = −0.419, p = 0.006), while no such significance was found in females (p = 0.574 and p = 0.342). The analyses of the possible relations of serum BDNF concentration with the spirometric parameters in the whole group of patients did not reveal any significance (p = 0.231 for FEV1%pr. and p = 0.271 for FEV1/FVC%). However, when the patients were dichotomized on the basis of smoking habits, we obtained a strong positive correlation between BDNF and FEV1%pr. (Rho = 0.501, p = 0.048) in non-smokers, but strong negative correlations with FEV1%pr. (Rho = −0.468, p = 0.003) and with FEV1/FVC% (Rho = −0.331, p = 0.040) in ex/current smokers. Non-smokers with moderate disease (GOLD II) had higher BDNF serum concentrations than patients with GOLD stage III/IV (p = 0.031). In ex/current smokers, there was an opposite association (p = 0.045). Conclusions: The results of our study suggest that the expression and secretion of BDNF are changed in COPD, but its effects and functions may differ according to the smoking history of the patients.

Background and Objectives: Glioblastoma (GBM) is the most aggressive primary tumor of the central nervous system, characterized by high invasiveness and poor prognosis. Inflammation in the tumor microenvironment, including the presence of immunosuppressive M2-macrophages (CD163+), plays a key role in disease progression. The aim of this study was to evaluate serum levels of interleukin-22 (IL-22) in Bulgarian patients with GBM and to analyze its diagnostic role, its relationship with systemic inflammatory markers (NLR), metabolic parameters, and the infiltration of CD163+ cells. Materials and Methods: The study included 41 newly diagnosed patients with GBM and 46 healthy controls. Serum IL-22 levels were measured by ELISA, and the density of CD163+ cells in the tumor tissue was analyzed immunohistochemically. Statistical analysis included Mann–Whitney test, ROC analysis, binary logistic regression, and Kaplan–Meier survival analysis. Results: GBM patients showed significantly higher levels of IL-22 compared to healthy controls (p = 0.001). ROC analysis demonstrated moderate diagnostic ability of IL-22 (AUC = 0.713), with high levels being a potential risk factor for the disease (OR= 2.51). A weak inverse correlation was found between IL-22 and neutrophil-to-lymphocyte ratio (NLR) (p = 0.048). Although IL-22 levels alone did not affect overall survival, patients with high levels of the cytokine and dense stromal infiltration of CD163+ macrophages tended to have shorter overall survival (p = 0.080). Conclusions: IL-22 is a potential diagnostic biomarker, probably reflecting the systemic inflammatory response in GBM. Its prognostic value might be contextually dependent on the tumor microenvironment, as high levels of IL-22 in combination with immunosuppressive macrophages may contribute to a more aggressive course of the disease.

Background: COPD is a multifactorial chronic lung disease driven by an abnormal inflammatory reaction. It is well recognized that genetic factors play a role in susceptibility to COPD. Hence, polymorphism in pro-inflammatory cytokines, including interleukin-1 (IL-1), may confer a risk for the development of COPD. Methods: We genotyped 163 patients with COPD and 174 control individuals using a TaqMan genotyping assay for IL1B -511 C>T SNP and a PCR-RFLP-based method for IL1B +3953 C>T SNP and VNTR polymorphism in IL1RN in order to elucidate their possible role as candidate risk factors of COPD in a Bulgarian population. Results: The genotypes containing at least one variant T allele of IL1B -511 C>T SNP demonstrated a 2.1-fold higher risk for COPD after adjustment for age, sex, and smoking status (p = 0.011). The genotype with at least one T allele of IL1B +3953 C>T appeared to be protective, with a 2.21-fold lower risk for COPD after adjustment for sex, age, and smoking status (p = 0.007). The IL1B T_C haplotype showed a 1.70-fold higher risk of COPD (p = 0.018) in comparison to the C_T haplotype. Carriers of the VNTR IL1RN 1*3 genotype develop COPD earlier compared to 1*1 (p = 0.099). Patients with the 2*2 genotype had slightly higher FEV1/FVC (%) in comparison to 1*2 carriers (p = 0.09). Conclusions: To our knowledge, this study is the first to provide exploratory evidence on the T_C haplotype of IL1B -511 C>T; +3953 C>T that may be a predisposing factor for COPD in Bulgarian population. We suggest that the VNTR polymorphism of the IL1RN gene does not affect the risk for COPD but may lead to early disease development.