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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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-γ 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 thoracenthesis 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-γ level in pleural fluid was measured with commercially available immunoenzymatic assay (Quantikine Human IFN-γ 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-γ 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. Conclusions: The pleural fluid concentration of IFN-γ was found to be highly sensitive and specific marker of tuberculous pleurisy.

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Astma wiąże się z napływem eozynofilów do dróg oddechowych. Eozynofile odgrywają ważną rolę w patogenezie tej choroby. Interleukina-5 jest głównym czynnikiem regulującym proliferację, dojrzewanie i dystrybucję eozynofilów, mimo że ostatnie badania sugerują, że poza IL-5 w patogenezie astmy może uczestniczyć eotaksyna. Eotaksyna jest CC chemokiną po raz pierwszy odkrytą w płynie z płukania oskrzelikowo-pęcherzykowego u świnki morskiej. Eotaksyna łączy się selektywnie z receptorem CCR3 obecnym na eozynofilach, bazofilach i mastocytach, co może wiązać się z patogenezą astmy. Jest ona wytwarzana przez komórki nabłonka płuc i jelit, pośredniczy w preferencyjnej rekrutacji eozynofilów do tych organów. Produkcję eotaksyny stymuluje IL-4, IL-13, TNF-α. Obecnie znane są trzy eotaksyny ludzkie: eotaksyna-1 (CCL11), eotaksyna- 2 (CCL24) i eotaksyna-3 (CCL26). Przypuszcza się, że ekspresja eotaksyny-3 może być następstwem prowokacji alergenowej. W badaniach na hodowlach komórkowych in vitro wykazano pewne działanie hamujące glikokortykosteroidów na produkcję eotaksyn. Danych klinicznych dotyczących wpływu leczenia kortykosteroidami na stężenie eotaksyn nie ma zbyt wiele. Receptor CCR3 bierze się pod uwagę jako cel terapeutyczny w astmie oskrzelowej.

Rationale: Weight loss and cachexia are relevant systemic manifestations of chronic obstructive pulmonary disease (COPD) and belong to the negative prognostic factors in this disease. The aim of our study was to analyze body composition and serum leptin and adiponectin in COPD patients categorized according to the GOLD stage (II-IV) . Material :The study group consisted of 67 COPD patients (43 M, and 24 F, at mean age 68.2±8 yrs, and FEV of 51.6±14.2% pred.). There 1 were 33 patients in GOLD II, 23 patients in GOLD III and 11 patients in GOLD IV stage, respectively. 12 patients were current smokers and the cumulative tobacco exposure for the whole group was 40.2± 18.7 pack-years. Methods: Body composition was analyzed by bioelectric impendence with Tanita T5896 balance. All patients had also undergone spirometry and body plethysmography (Vmax V6200 Autobox) and 6-minute walk test (6MWT), leptin and adiponectin was measured using the ELISE test (R&D Systems). Results:3. Basal metabolic rate (BMR) decreases with COPD severity and correlates with lung hyperinflation This abstract is funded by: National Center for Science and Progress ( NCBiR) Poland Am J Respir Crit Care Med 185;2012:A4515 Internet address: www.atsjournals.org Online Abstracts Issue

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