Background Th2 cells play an important role in intermittent allergic rhinitis (IAR). Interleukin (IL)-33 stimulates the production of Th2-associated cytokines. IL-33 binds to ST2 receptor which is highly expressed on mast cells and selectively on Th2 cells. IL-33 and ST2 might be involved in the Th2-mediated immune response. Objective We analyzed the serum level of IL-33 and its receptor ST2 in patients with IAR sensitive to grass and/or tree pollen to assess if the serum level of IL-33 and/or ST2 may be a marker of the disease severity. Methods IL-33, ST2 and total immunoglobulin (Ig) E were measured in sera of patients with IAR sensitive to birch and/or grass pollen and in patients with controlled bronchial asthma and in non-allergic controls. IAR severity was assessed by total nasal symptom score. Results Serum levels of IL-33 in patients with IAR were comparable with patients with bronchial asthma and were significantly higher in patients with IAR (P = 0.0035) and in patients with bronchial asthma (P = 0.008) than in controls. Serum levels of IL-33 correlated with disease severity. Conclusion Elevated level of IL-33 in sera of patients with IAR sensitive to tree and/or grass pollen and the correlation of IL-33 with the disease severity suggest that IL-33 is involved in the pathogenesis of intermittent allergic rhinitis.

Background: Epithelium-derived cytokines such as thymic stromal lymphopoietin (TSLP), interleukin (IL)-25, and IL-33 are important contributors to inflammation in asthma. Exhaled breath condensate (EBC) is a noninvasive method used to assess the inflammation of airways. Our aim was to assess the levels of TSLP, IL-25, IL-33, and its receptor ST2l/IL-1 R4 in EBC in patients with asthma and to correlate these with serum levels and asthma control. Methods: EBC and serum levels of TSLP, IL-25, IL-33, and ST2l/IL-1 R4 were measured in 44 patients with chronic bronchial asthma (14 in the uncontrolled phase) and 19 healthy control participants. Results: EBC levels of IL-33 and TSLP and serum levels of IL-33 were statistically higher in patients with asthma than in controls. IL-25 and ST2l/IL-1 R4 were present in EBC at barely detectable levels and were not analyzed. The EBC and serum levels of all studied mediators did not differ between controlled and uncontrolled asthma patients, except for the serum level of ST2l/IL-1 R4, which was higher in uncontrolled asthma. There were no correlations between serum and EBC levels of TSLP and IL-33 or between either serum and EBC levels and the forced expiratory volume in 1 s or the total IgE level. Conclusions: Higher levels of IL-33 and TSLP in EBC provide evidence supporting a role for these mediators in asthma. Their levels do not discriminate between controlled and uncontrolled asthma. The local reaction within the epithelium is independent of the systemic reaction.

IL-33, a member of the IL-1 cytokine family and a ligand to receptor ST2, has great potential to induce a T helper 2-type inflammatory response. IL-33 is proven to be released by epithelial cells during their injury by different environmental stimuli such as airborne allergens, viruses, and air pollutants. IL-33 acting as an endogenous danger signal is termed an alarmin. As such, this cytokine is considered to play a crucial role in an allergic inflammatory disease such as rhinitis. Recent investigations regarding the IL-33/ST2 axis involvement in Th2 inflammatory response and pathogenesis of rhinitis have been reviewed. The role of IL-33 as a novel promising therapeutic target has also been discussed.

Introduction : The pathogenesis of asthma remains unclear, especially in cases of the severe disease. Aim : To explore IgE-mediated inhalant sensitization in severe asthma compared with a group of patients with chronic mild disease and evaluate the Th1/Th2 cytokine profiles in asthma by...

Background: There is a need for searching for biomarkers indicating patients who will benefit the most from treatment with omalizumab for chronic spontaneous urticaria (CSU). The aim of this study was to assess whether the eosinophil/neutrophil/platelet/basophil-to-lymphocyte ratio (ELR, NLR, PLR, BLR) may predict the response to omalizumab treatment of chronic spontaneous urticaria. Methods: A retrospective data analysis of CSU patients treated s-c with 300 mg of omalizumab every four weeks under the drug program was carried out. NLR, ELR, PLR and BLR, DLQI, UAS-7, CRP, anti-TPO and tIgE were assessed before (V0) and after three (V3) and six months (V6) of treatment. Results: Among 52 patients with CSU, 21 were responders, 24 were partially responders and 6 were non-responders to treatment with 300 mg omalizumab every four weeks. An amount of 18 patients had features of type I autoallergic CSU (CSU^aiTI) and 34 patients had autoimmunity type IIb CSU with mast cell-directed activating autoantibodies (CSU^aiTIIb). NLR, ELR, PLR and BLR indices did not change during a six-month-course of biological treatment. Initial values of ELR and BLR were significantly correlated with the initial tIgE level and anti-TPO/IgE ratio. Initial values of NLR, ELR and BLR were significantly correlated with initial CRP. Comparisons between type I autoallergic CSU (CSU^aiTI) and autoimmunity type IIb CSU (CSU^aiTIIb) revealed that the absolute number and percentage of eosinophils, basophils, BLR and tIgE were significantly higher in type CSU^aiTI and anti-TPO and anti-TPO/IgE were significantly lower in type CSU^aiTI. Conclusions: NLR, ELR, PLR and BLR do not change significantly during six months of omalizumab treatment and do not appear to be useful in predicting its efficacy.

Allergic fungal rhinosinusitis (AFRS) is primary, Th2-mediated, chronic rhinosinusitis, which is diagnosed when the criteria defined by Bent and Khun are met. The disease is most common in countries located in the subtropical and tropical regions characterized by high temperatures and high levels of humidity, which favour the wider occurrence of fungi in the environment. The presence of specific IgE antibodies directed against fungal allergens, which is one of the diagnostic criteria, proves the systemic nature of the disease and allows one to distinguish AFRS from eosinophilic fungal rhinosinusitis. There is no unified treatment method for AFRS described in the literature, and relapses are common. Sinus surgery remains the treatment of choice. Oral and topical steroid therapy plays an important role in the treatment process. The effectiveness of antifungal treatment and immunotherapy is unclear. Biological treatment, the results of which are promising, has raised great hopes. The aim of this study was to reveal how often AFRS occurs in European countries, what environmental factors influence its development, and how important it is to specify its diagnostic criteria and treatment methods. We present an overview of the available literature. In addition, we share our own experience and describe two cases of AFRS diagnosed and treated at our centre.