Iskanje po repozitoriju

A+ | A- | | SLO | ENG

Povzetek: Children with autism spectrum disorder (ASD) exhibit gut mucosal immune alterations, but the co-regulatory architecture linking stool immune proteins and cytokines within the same cohort remains unstudied. In 115 children (74 ASD, 41 controls; age 5–18 years), seven stool immune proteins (IgA subclasses, α1-antitrypsin and calprotectin subunits) were quantified by UHPLC-MS/MS and ten by Luminex—chemokines eotaxin/CCL11 and IL-8/CXCL8 plus eight cytokines—each normalised to total protein. Age-adjusted partial Spearman correlations were computed for all 70 protein–cytokine pairs per stratum, using Benjamini–Hochberg correction, bootstrap confidence intervals and Fisher r-to-z tests. No pair survived FDR correction in any stratum. IgA1 and IL-1β/TP correlated positively across all strata (full cohort ρ = 0.409, 95% CI 0.131–0.634, n = 62; controls 0.583; ASD 0.210), with no significant between-group difference (Fisher z = 1.70, p = 0.090). Multiple imputation attenuated this to ρ = 0.265 (95% CI 0.055–0.452). An inverse trend between IL-1β/TP and CARS score (ρ = −0.336, n = 41) did not survive correction (p-FDR = 0.576). This power-limited, hypothesis-generating study identifies an exploratory IgA1–IL-1β mucosal axis present across groups, with no confirmed between-group difference. Adequately powered multi-centre studies are required.
Ključne besede: autism spectrum disorder, stool proteomics, cytokines, IgA, calprotectin, alpha-1-antitrypsin, IL-1β, gut mucosal immunity, partial Spearman correlation, Luminex
Objavljeno v DiRROS: 12.08.2026; Ogledov: 264; Prenosov: 131
Celotno besedilo (604,78 KB)
Gradivo ima več datotek! Več...

Povzetek: Background: Bronchopulmonary dysplasia (BPD) is a leading chronic lung complication in extremely premature newborns. The etiological factors contributing to of BPD include both prenatal and postnatal risk factors, as well as activation of innate immunity. Innate immunity and its bioactive mediators play a central role in orchestrating the inflammatory response. Among these, interleukin-1β (IL-1 β) and IL-8 (CXCL8) are particularly prominent. Methods: A structured literature search was conducted across major biomedical databases (PubMed, Scopus, Web of Science, and Ovid MEDLINE) to identify relevant studies published between 1993 and November 2025. Article selection was guided by predefined inclusion criteria focusing on studies that examined IL-1β and IL-8 (CXCL8) in relation to bronchopulmonary dysplasia. Evidence from both human and animal studies was narratively synthesized. Results: This review provides a detailed description of the role of the innate immune system in BPD, including mechanisms of inflammatory initiation, evidence from human and animal studies on IL-1β and IL-8 (CXCL8), and the interaction between these two cytokines in the development of chronic lung disease. Conclusions: Both human and animal studies generally suggest that elevated levels of IL-1β and IL-8 (CXCL8) are closely associated with the development of bronchopulmonary dysplasia in premature infants.
Ključne besede: premature infant, chronic lung disease, inflammation, cytokines, chemokines
Objavljeno v DiRROS: 22.07.2026; Ogledov: 265; Prenosov: 154
Celotno besedilo (1,92 MB)
Gradivo ima več datotek! Več...

Povzetek: Glioblastoma (GB) is an aggressive primary brain cancer with poor patient prognosis. Natural killer (NK) cells can recognise and eliminate a range of malignant cells, including GB stem cells, which drive GB recurrence. NK cell-based immunotherapy has emerged as a promising approach for GB treatment, but a better understanding of the complex crosstalk between GB and NK cells is needed, particularly within the immunosuppressive GB tumour microenvironment. In this study, we established a reproducible protocol for the production and dynamic culture of uniformly sized GB spheroids using the Celvivo Clinostar system. Our spheroids recapitulated the heterogeneous structure of GB and expressed ligands for NK cell receptors at levels distinct from those observed in corresponding GB cell lines in standard culture, implicating altered sensitivity of GB cells to NK cells in dynamic 3D cultures. GB-NK cell crosstalk was GB cell type dependent and the ability of NK cells to infiltrate GB did not necessarily correlate with their cytotoxicity against GB cells. Spheroids derived from differentiated GB cells secreted higher levels of immunomodulatory cytokines compared to spheroids from GB stem-like cells, and a prominent increase in the secretion of immune-attracting factors was observed in their co-cultures with NK cells. Finally, the CD155-DNAM1/TIGIT axis was indicated as an important regulator of NK cell cytotoxicity against GB stem-like cells. Collectively, our results highlight important factors in GB-NK cell communication and provide a groundwork for further targeted research as well as therapeutic evaluation of NK cell-based approaches in the established dynamic 3D cultures.
Ključne besede: glioblastoma, immunotherapy, dynamic in vitro models, natural killer cells, cytotoxicity, 21 infiltration, cytokines, CD155
Objavljeno v DiRROS: 11.06.2026; Ogledov: 361; Prenosov: 294
Celotno besedilo (6,86 MB)
Gradivo ima več datotek! Več...

Povzetek: Objective: To determine the dynamics of serum levels of TNF-α in patients with juvenile idiopathic arthritis (JIA) treated with anti-TNF-α biological drugs and investigate their association with the disease activity. Methods: We conducted a single-centre, observational cohort study in 98 patients with JIA (30 boys, 68 girls, mean age 11.3 years) treated with anti-TNF-α biological drugs. Clinical examinations and laboratory assessments of serum levels of TNF-α were performed before starting therapy with biological drug and at 6-month intervals afterwards up to 2.5 years. Results: The analysis of serum levels of TNF-α in relation to the disease activity states showed the highest mean serum levels of TNF-α in patients on etanercept who had low disease activity states and in patients on adalimumab who had inactive disease. The correlation analysis in patients with JIA treated with etanercept or adalimumab showed a weak negative correlation between the serum levels of TNF-α and JADAS10 scores (p = 0.007), (r = - 0.177). Conclusion: The assessment of serum levels of TNF-α in children with JIA during treatment with etanercept or adalimumab is not a reliable biomarker of disease activity or immunological remission. Longitudinal measurement of TNF-α has no added clinical value in patients with JIA treated with anti-TNF-α biological drugs. Key Points • There is limited evidence regarding the effect of anti-TNF therapy on serum concentrations of TNF-α in patients with juvenile idiopathic arthritis • Our study showed an increase in the serum level of TNF-α after the initiation of therapy with either etanercept or adalimumab, which was more significant in patients with inactive or low disease activity • Serum TNF-α is most likely not biologically active during therapy with TNF-α inhibitors and therefore not a reliable biomarker of disease activity or immunological remission in patients with juvenile idiopathic arthritis
Ključne besede: adalimumab, cytokines, etanercept, juvenile idiopathic arthritis, tumour necrosis factor-alpha
Objavljeno v DiRROS: 05.06.2026; Ogledov: 328; Prenosov: 127
Celotno besedilo (966,01 KB)

Povzetek: This narrative review examines degenerative disc disease (DDD), a major cause of chronic back pain and disability worldwide. It is a multifactorial condition resulting from a complex interplay of genetic, mechanical, metabolic, and environmental factors that progressively impair disc structure and function. The pathophysiology of DDD involves disruption of extracellular matrix homeostasis, cellular senescence, oxidative stress, and chronic inflammation mediated by cytokines such as IL-1β, TNF-α, and IL-6. These processes are further modulated by signalling pathways including NF-κB, MAPK, and Wnt/β-catenin, leading to matrix degradation, dehydration, and loss of disc height. Epidemiological studies highlight the contribution of lifestyle and metabolic disorders, such as obesity, smoking, and diabetes, to disease progression. Traditional conservative and surgical treatments primarily alleviate symptoms but do not halt or reverse degeneration. In contrast, recent advances in molecular biology and regenerative medicine have opened new therapeutic avenues. Mesenchymal stem cell therapy, biomaterial scaffolds, and gene-based interventions aim to restore disc homeostasis by promoting matrix synthesis and suppressing catabolic activity. Despite promising experimental results, clinical translation remains limited by challenges in cell viability, delivery methods, and long-term efficacy. Future research integrating molecular, biomechanical, and regenerative strategies offers the potential for true biological repair and disc regeneration.
Ključne besede: intervertebral disc, degenerative disc disease, oxidative stress, cytokines, cellular senescence
Objavljeno v DiRROS: 08.04.2026; Ogledov: 385; Prenosov: 300
Celotno besedilo (1,96 MB)
Gradivo ima več datotek! Več...