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Background: Asthma is a frequent chronic disease of the airways. In spite of the fact that symptoms of asthma are well known, the pathogenesis has not yet been fully understood. Quantitative computed tomography (qCT) of the lung allows for the measurment of a set of parameters. The aim of this study was to evaluate the usefulness of quantitative computed tomography in the assessment of airway wall thickness in asthma. Methods: The prospective study was performed on a group of 83 patients with well-defined, long-term asthma between 2016 and 2018. The control group was composed of 30 healthy volunteers. All examined subjects were non-smokers. All computed tomography (CT) studies were performed using a 128 multi-slice CT scanner with no contrast, following a chest scanning protocol in the supine position, at full inspiration and breath-holds. Results: Quantitative bronchial tree measurements were obtained from the third up to the ninth generation of the posterior basal bronchi (B10) of the right lung in a blinded fashion. The value of the wall thickness in patients with asthma was significantly higher in all measured generations of the bronchial tree (third to ninth generation). The lumen area and the inner diameter significantly correlated with the lung function tests and were substantially smaller in the examined group from the seventh to the ninth generation of the bronchi ( p < 0.05). Conclusions: We conclude that airway remodelling occurs in most patients with long-term asthma and is associated mainly with the medium and small airways. Imaging techniques, especially qCT can be useful in the diagnosis and management of asthma. The reviews of this paper are available via the supplemental material section.

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Recent years of research have shed a new light on the role of IgE in immune reactions. It seems to be more than just a contribution to immediate type of allergic response. It appears that monomeric IgE may enhance mast cell activity without cross-linking of FcεRI by IgE specific allergen or autoreactive IgG anti-IgE antibodies. Monomeric IgE molecules are heterogeneous concerning their ability to induce survival and activation of mast cells only by binding the IgE to FcεRI, but not affecting degranulation of cells. It also turned out that IgE may react to autoantigens occurring in the blood not only in chronic spontaneous urticaria (CSU) but also in other autoimmune diseases. The aforementioned phenomena may promote the activity of mast cells/basophils in CSU that easily degranulate when influenced by various inner (autoreactive IgG against IgE and FcεRI, autoreactive IgE for self-antigens) and outer factors (cold, heat, pressure) or allergens. These findings forced the new approach to the role of autoimmunity, self-antigens and IgE autoantibodies in the pathology of CSU. CSU put in the scheme of autoreactive IgG and autoreactive IgE seems to be either a kind of an autoimmune disease or a clinical manifestation of some other defined autoimmune diseases or both.

Background: The CTLA-4 molecule is an important negative regulator of T cell activation. It is encoded on chromosome 2q33 and found to be associated with several allergic phenotypes including asthma. However, the association of CTLA-4 gene polymorphisms with allergic asthma is still controversial and therefore was the subject of this study. Methods: By PCR-RFLP, the distribution of three single nucleotide polymorphisms (SNPs), –1147 C/T, –318 C/T, and +49 A/G, was examined in 219 Polish Caucasoid patients diagnosed with allergic asthma and in 102 ethnically matched healthy control individuals. (AT)_n microsatellite polymorphism was also tested in the same individuals. Results:No statistically significant differences in SNPs or microsatellite allele, genotype or haplotype frequencies between patients and controls were found. Conclusion:CTLA-4 polymorphisms do not seem to be a risk factor for allergic asthma in Poles.