Expression of eotaxins in the material from nasal brushing in asthma, allergic rhinitis and COPD patients.

BACKGROUND: Asthma and COPD are non-infectious inflammatory diseases of the respiratory tract. Allergic rhinitis can be assumed as an intermediate condition between healthy and asthmatic state. Eotaxins are important indicators of allergic reaction. They are strong chemoattractants mainly for eosinophils but also for other cells. OBJECTIVE: We measured the level of eotaxin expression and inflammatory cell count in the material from nasal brushing in healthy controls and in patients with allergic rhinitis, asthma, and COPD. We studied the correlation between the eotaxin gene expression level in the material from nasal brushing and respiratory tests in asthma and COPD patients. METHODS: Expression of eotaxins was measured using quantitative RT-PCR. Number of eotaxin transcript copies was evaluated using real time PCR standard curve method. RESULTS: Of all eotaxins CCL24 had the highest expression in the material from nasal brushing, and its level was increased in allergic asthma. CCL11 was significantly increased in the material from nasal brushing of COPD patients. Increased levels of all three eotaxins were observed in the material from nasal brushing of patients with allergic rhinitis in season. The levels of CCL26 expression and FEV1/FVC factor were correlated negatively in the asthma group and positively in the COPD group. CONCLUSIONS: Eotaxins are crucial factors of allergic, asthmatic and also COPD inflammatory reactions. Our results suggest a dual role of CCL26 - it can act as a negative regulator for neutrophils in COPD, while in asthma it may act as a chemoatractant of eosinophils and other cells into the lung.

IL-6 and IL-13 in induced sputum of COPD and asthma patients: correlation with respiratory tests.

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 FEV(1) or FEV(1)/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 FEV(1), FEV(1)% 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.

Analysis of eotaxin 1/CCL11, eotaxin 2/CCL24 and eotaxin 3/CCL26 expression in lesional and non-lesional skin of patients with atopic dermatitis.

UNLABELLED: Eotaxins are the chemokines which are highly selective chemotactic agents for eosinophils. The aim of our study was the evaluation of the gene expression level for eotaxin 1/CCL11, eotaxin 2/CCL24, and eotaxin 3/CCL26, both in skin changes and in uninvolved skin of atopic dermatitis (AD) patients. The study comprised 19 patients with AD and 10 healthy controls. The gene expression level for eotaxins in the skin biopsies was evaluated by the real-time quantitative PCR. The change of the gene expression level, calculated as log10 skin lesions/non-lesional skin, was 0.635 for CCL11, 0.172 for CCL24 and 0.291 for CCL26. The change of the gene expression level, calculated as log10 non-lesional skin of AD patients/healthy control, was 0.394 for CCL11, -0.216 for CCL24, and 0.229 for CCL26, while skin lesions of AD patients/healthy control, was: 0.788, -0.046, and 0.483, respectively. CONCLUSION: The mean gene expression level for CCL11, CCL24, CCL26 was higher in skin changes of AD patients than in uninvolved skin. The higher level of CCL26 in skin changes, indicates its role in their aetiology in AD. The gene expression level for CCL24 in AD patients was lower, both in involved and uninvolved skin vs. the healthy control.

[Pleural fluid interferon-gamma (IFN-gamma) measurement as a diagnostic tool in tuberculous pleurisy]. / Przydatnosc oznaczania interferonu gamma (IFN-gamma) w plynie z oplucnej w diagnostyce gruzliczego wysiekowego zapalenia oplucnej.

INTRODUCTION: Tuberculosis is one of the most common causes of pleural effusion (PE). However, the diagnosis of tuberculous pleurisy still remains difficult. Since M. tuberculosis isolation rates in tuberculous effusions are relatively low the histological and microbiological studies of pleural biopsy samples are usually required to confirm the diagnosis. Several biological markers have been proposed to enhance the effectiveness of diagnosing patients with tuberculous pleurisy. The study was undertaken to evaluate the diagnostic accuracy of pleural fluid IFN-gamma concentration in differentiation between tuberculous pleural effusion (TPE) and non-tuberculous pleural effusion (nTPE). MATERIAL AND METHODS: 94 patients (50 M and 44 F, mean age 59 +/- 18, range 18-95 years) with PE were studied. All subjects underwent diagnostic thoracentesis and extensive laboratory pleural fluid evaluation. Tuberculous pleural effusion was diagnosed in: 1) patients with positive pleural fluid or pleural biopsy culture and 2) patients with granulomas in the pleural biopsy specimen, after exclusion of other granulomatous diseases. IFN-gamma level in pleural fluid was measured with commercially available immunoenzymatic assay (Quantikine Human IFN-gamma Immunoassay, R&D Systems, USA). RESULTS: Tuberculous pleural effusion was diagnosed in 28 pts. The non-tuberculous pleural effusion group consisted of 66 pts, including 35 with malignant PE, 20 with parapneumonic effusion or pleural empyema, 5 with pleural transudates due to heart failure, and 6 with miscellaneous causes of PE. The mean concentration of IFN-g was significantly higher in TPE than in nTPE (614.1 +/- 324.5 vs. 15.1 +/- 36.0 pg/ml, p < 0.0001). At the cut-off value of 100 pg/ml the sensitivity and specificity of the test were 100% and 98,5% respectively. CONCLUSION: The pleural fluid concentration of IFN-gamma was found to be highly sensitive and specific marker of tuberculous pleurisy.

[Role of eotaxin in the pathophysiology of asthma]. / Rola eotaksyn w patofizjologii astmy.

Asthma is associated with eosinophilic airway inflammation and eosinophils are believed to be important in the pathogenesis of asthma. IL-5 has been considered the central mediator for eosinophilic proliferation, differentiation and eosinophilic inflammation, but results of recent studies suggest that besides IL-5, eotaxin may contribute to the pathogenesis of asthma. Eotaxin is CC chemokine first isolated from guinea pig bronchoalveolar lavage. It selectively binds to a specific receptor (CCR3) highly expressed on eosinophils, basophils, and mast cells being important in the pathogenesis of asthma. Eotaxin is produced mainly by epithelial cells of lung and gut, to mediate organ preferential attraction of eosinophils. Production of eotaxin is stimulated by IL-4, IL-13, TNF(-alpha). Human eotaxin family includes: eotaxin-1 (CCL11), eotaxin-2 (CCL24) and eotaxin-3 (CCL26). It seems that eotaxin-3 may be expressed following allergen challenge. Studies with glucocorticosteroids have shown some inhibitory effect on eotaxin production in cell culture in vitro however, very little in vivo data exists in humans relating to corticosteroid effects on chemokine levels. CCR3 receptor is considered as the possible therapeutic target in asthma treatment.