Background: IL-6 is strongly implicated in the development of chronic obstructive pulmonary disease (COPD). IL-13 is the well-documented central mediator in allergic asthma. IL-6 is attributed to the proinflammatory activities in COPD as well as asthma. In COPD patients exacerbation is increased by serum IL-6. The association of IL-13 as well as IL-6 with the impaired respiratory function of asthma patients remains controversial. Objectives: The aim of this study was to compare the concentration of IL-6 and IL-13 in the induced sputum of asthma and COPD patients, and to assess the possible association of these cytokines with the impairment of lung function. Methods: Twenty-six subjects with COPD and 18 subjects with asthma were enrolled in this study. IL-6 and IL-13 levels were measured in induced sputum by ELISA and correlated with the results of respiratory tests. Results: The induced sputum of COPD patients had a significantly higher IL-6 level than the sputum of asthma subjects while no significant differences were found in the levels of IL-13. There was a statistically significant negative correlation between IL-6 level and FEV₁ or FEV₁/FVC in asthma patients (r = –0.59 and –0.54, respectively) and a negative correlation that did not reach statistical significance between IL-6 level and FEV₁, FEV₁% or FVC in COPD subjects (r = –0.30, –0.30 and –0.38, respectively). There was no relationship between concentrations of IL-13 and impaired respiratory function. Conclusions: Our results confirmed that IL-6, but not of IL-13, is associated with respiratory disorders in both asthma and COPD patients.

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Asthma and COPD are the most common obstructive lung diseases characterized by inflammation in the lower airways which contribute to airflow limitation. Different inflammatory mediators are thought to play a key role in these diseases. This study was conducted in 13 patients with asthma, 12 patients with COPD, and 13 control subjects. The expression of mRNA of IL-6, IL-13, CXCL8, TSLP, IL-33, IL-25, IL-17, ECP, mast cell tryptase, CCL24, and CCL26 was assessed in induced sputum cells by real time PCR. We found that CXCL8 was strongly related to the neutrophil percentage but differed significantly in COPD and asthma patients. The expression of IL-17 was lower in patients with atopic asthma compared to non-atopic asthma. The percentage of macrophages correlated negatively with the expression of mast cell tryptase and ECP in COPD, and with CXCL8 in asthma. The expression of ECP correlated negatively with the severity of COPD symptoms measured by CAT. We conclude that asthma and COPD demonstrate a significant overlap in the airway cytokine profile. Thus, differentiation between the two diseases is difficult as based on a single cytokine, which suggests the coexistence of phenotypes sharing a common cytokine network in these obstructive lung diseases.

Bronchial hyperresponsiveness is a typical, but non-specific feature of cough variant asthma (CVA). This study aimed to determine whether bronchial hyperresponsiveness may be considered as a predictor of CVA in non-smoking adults with chronic cough (CC). The study included 55 patients with CC and bronchial hyperresponsiveness confirmed in the methacholine provocation test, in whom an anti-asthmatic, gradually intensified treatment was introduced. The diagnosis of CVA was established if the improvement in cough severity and cough-related quality of life in LCQ were noted.The study showed a high positive predictive value of bronchial hyperresponsiveness in this population. Cough severity and cough related quality of life were not related to the severity of bronchial hyperresponsiveness in CVA patients. A poor treatment outcome was related to a low baseline capsaicin threshold and the occurrence of gastroesophageal reflux-related symptoms. In conclusion, bronchial hyperresponsiveness could be considered as a predictor of cough variant asthma in non-smoking adults with CC.

Purpose Upper airway cough syndrome (UACS), described as chronic cough (CC) associated with allergic (AR), non-allergic rhinitis (NAR) or chronic rhinosinusitis (CRS), is one of the major causes of CC. We aimed to characterize a cohort of UACS patients with special attention to differences between patients with AR and NAR. Methods A prospective analysis of clinical data of patients, diagnosed with UACS between 2015 and 2018. Results There were 143 patients diagnosed with UACS, median age 52 years, women predominance (68.5%), The group comprised of 59 (41%) AR and 84 (59%) NAR subjects, CRS diagnosed in 17 (12%). Median cough duration: 48 months (IQR 24–120), median cough severity (VAS)—60 mm (IQR 42–78), median Leicester Cough Questionnaire (LCQ) score—11.3 (IQR 8.7–13.7), never-smokers: 70%. The most common symptoms: PND (62%), rhinorrhea (59%), nasal congestion (54%), abnormalities of sinus CT: septum deviation (62%), turbinates hypertrophy (53%), mucosal thickening (53%). UACS as the only cause of CC, was presented in 20 patients (14%). We found no differences between patients with AR and NAR in terms of age, gender, duration and severity of cough, BMI, blood eosinophil count, total IgE and FeNO. AR was associated with higher comorbidity of asthma than NAR (54% vs 35%, p = 0.019). Abnormalities in sinus CT scan were more frequently found in patients with NAR than AR (p = 0.018). Conclusion NAR is the most common upper airway disease associated with UACS. Clinical characteristics of UACS patients with AR and NAR are similar with only minor differences between these groups. It seems reasonable to plan further studies concerning relationship of NAR and cough sensitivity, also in terms of potential similar neurogenic mechanism.