Scientific publications

The cytokine concentration may be related to the level of inflammation and clinical features of diseases. The study was aimed to evaluate blood plasma level for TNFα, sTNFRII, IL-1β, IL-10 and FOXP3 gene expression in patients with different clinical forms of pulmonary sarcoidosis.
Materials and methods. Patients with pulmonary sarcoidosis (PS) enrolled in the study were characterized by chronic, progressive and active forms at PS stage 2. Control group was formed by conditionally healthy individuals. The cytokine (TNFα, sTNFRII, IL-1β, IL-10) concentration was examined by enzyme-linked immunosorbent assay (ELISA). Real-time polymerase chain reaction (RT-PCR) was used to analyze FOXP3 gene expression in peripheral blood leukocytes (PBL).
Results. The high levels of plasma TNFα and sTNFRII were detected in patients with progressive and active PS vs chronic PS (p = 0.0263, p = 0.0321 and p = 0.0012, p = 0.0009, respectively). Concentration of IL-1β was higher in active PS rather than in chronic and progressive PS (p = 0.0002 and p = 0.0020, respectively). The IL-10 plasma level in patients from all studied groups was lower compare to healthy individuals (p = 0.0009, p = 0.00009, p = 0.0004, respectively). A decreased number of PBL FOXP3 gene transcripts was found in patients with progressive and active PS (p = 0.0008 compared with healthy individuals and patients with chronic PS).
Conclusion. The level of cytokines in patients with PS is determined by disease clinical features. Upregulated proinflammatory factor (TNFα, sTNFRII, IL-1β) level as well as downregulated FOXP3 gene expression and the IL-10 concentration may suggest about potentiated inflammatory reactions in patients with progressive and active PS. To clarify disease clinical presentation, it is crucial to gain more information about the molecular biomarker dynamics mirroring magnitude of inflammation in PS. In addition, it is also required to propose proper therapy and its refinement. Moreover, the data obtained can be used to assess pathogenetic mechanisms underlying disease development and progression.