Analysis of changes in expression of IL-4/IL-13/STAT6 pathway and correlation with the selected clinical parameters in patients with atopic asthma.

INTRODUCTION: Asthma is associated with activation of interleukin-4 (IL-4)/interleukin-13 (IL-13)/signal transducer and activator of transcription factor-6(STAT6) inflammatory response via overexpression of all pathway components: IL-4, IL-13, and STAT6. OBJECTIVES: To evaluate the association of IL-4, IL-13, and STAT6 expression and immunoexpression with atopic asthma development. PATIENTS AND METHODS: Fifty patients with atopic asthma and 20 healthy controls were enrolled into the study. Relative gene expression was analyzed by qPCR method. Immunoexpression was assessed by ELISA method. RESULTS: The expression levels of IL-4, IL-13, and STAT6 were higher in patients compared to the controls, but a statistically significant difference was observed only for IL-13 (P = 0.03). In immunoexpression analysis, a statistically significant difference between patients and controls was found for IgE (P = 0.03). Significant positive correlations in the patient group were found between IL-13 gene expression and total level of serum IgE (rho = 0.230, P = 0.033), STAT6 gene/STAT6 protein and total level of serum IgE (STAT6: rho = 0.077, P = 0.038; STAT6: rho = 0.049, P = 0.042), IL-4, and STAT6 expression (rho = 0.098, P = 0.048). Any significant correlations were found between expression/immunoexpression levels of the studied genes and clinical classification, clinical features, or lung function parameters. CONCLUSIONS: Our data support the role of Th2 cytokines (IL-4, IL-13) and STAT6 in Th1/Th2 imbalance and highlight the etiological relationship between IL-4/IL-13/STAT6 signaling and atopy and asthma.

The Role of CXC Chemokines in Pulmonary Fibrosis of Systemic Lupus Erythematosus Patients.

The inflammatory process in systemic lupus erythematosus (SLE) affects many organs including the lungs. CXC chemokines are suggested to play an important role in the pathogenesis of SLE and pulmonary fibrosis. To estimate the concentrations of CXCL9, CXCL10, CXCL11 in bronchoalveolar lavage fluid (BALF) of patients with and without pulmonary involvements of SLE to evaluate CXC chemokines role in the pathogenesis of pulmonary fibrosis in SLE. Twenty-six SLE patients and 31 healthy controls were evaluated using high-resolution computed tomography (HRCT), pulmonary function tests, the SLE Disease Activity Index (SLEDAI), assessing CXCL9, CXCL11, CXCL10 level in BALF (an enzyme-immunosorbent assay kit). The mean CXCL9 and CXCL11 concentrations in BALF were higher in SLE patients compared to healthy controls (34.09 ± 102.34 vs 10.98 ± 14.65 pg/mL, p < 0.001; 72.65 ± 112.89 vs 16.12 ± 83.75 pg/mL, p = 0.012, respectively). The disease activity scored by SLEDAI and the concentration of CXCL10 in BALF were significantly higher in the SLE patients with pulmonary fibrosis when compared with patients with normal HRCT (8.23 ± 3.19 vs 5.01 ± 2.41; 73.45 ± 34.12 vs 40.76 ± 41.65, respectively, in both p < 0.05). In SLE patients positive correlations were found between SLEDAI and the percentage of lymphocytes in BALF (r = 0.51, p < 0.05); CXCL9 and CXCL10 concentrations in BALF (r = 0.65, p < 0.001); CXCL9 and CXCL11 concentrations in BALF (r = 0.69, p < 0.001). In lupus patients with pulmonary manifestations positive correlations were found between CXCL11 concentration in BALF and SLEDAI (r = 0.55, p < 0.05), CXCL11 concentration and the percentage of neutrophils in BALF (r = 0.69, p < 0.05), CXCL10 concentration and the percentage of neutrophils in BALF (r = 0.57, p < 0.05). Our observations indicate that CXCL9 and CXCL11 play an important role in the pathogenesis of SLE but it needs further studies. These results suggest that CXCL10 and CXCL11 are associated with neutrophils accumulation in the alveolar space of SLE patients with pulmonary fibrosis and should be considered as potential factor of interstitial fibrosis.

Evaluation of Markers of Inflammation and Oxidative Stress in COPD Patients with or without Cardiovascular Comorbidities.

BACKGROUND: Although both chronic obstructive pulmonary disease (COPD) and cardiovascular diseases (CVD) are characterised by chronic, systemic inflammation, their reciprocal interactions are poorly understood. The purpose of this study was to determine the concentrations of both inflammatory and oxidative stress biomarkers in the serum and exhaled breath condensate (EBC) of COPD patients, either with coexisting CVD or without cardio-vascular comorbidities. METHODS: Twenty-four COPD patients with CVD were allocated to group A, 20 COPD patients without CVD were assigned to group B and 16 healthy patients were included as a control. A medical history and physical examination were performed, and the following were measured: serum CRP concentration, glucose level, uraemic acid level and lipid profile. In addition 8-isoprostane, LTB4 and IL-8 concentrations were measured both in serum and EBC. Spirometry, six-minute walk test and echocardiography were performed in all subjects. RESULTS: EBC concentrations of 8-isoprostane and LTB4, and serum levels of CRP, 8-soprostane, LTB4, IL-8 were significantly higher in COPD patients than in healthy controls. COPD patients with CVD were not found to have higher concentrations of the assessed markers than those without CVD, neither in the serum nor EBC. CRP, 8-isoprostane and LTB4 levels in serum, and IL-8 concentration in EBC correlated negatively with the value of forced expiratory volume in one second. CONCLUSIONS: Although systemic inflammation coexists with COPD, it is not elevated in COPD patients with CVD. Since this phenomenon may result from treatment with statins, future studies should state whether COPD patients could benefit from the additional statin therapy.

Exhaled IL-8 in systemic lupus erythematosus with and without pulmonary fibrosis.

The purpose of this study is to evaluate the relationship between the concentration of interleukin-8 (IL-8) in exhaled breath condensate (EBC) and bronchoalveolar lavage fluid (BALF) with the disease activity score and pulmonary function of systemic lupus erythematosus (SLE) patients with and without pulmonary fibrosis. Thirty-four SLE patients and 31 healthy controls were enrolled and evaluated using high-resolution computed tomography (HRCT), pulmonary function tests, systemic lupus activity measure (SLAM), assessing BALF and EBC. IL-8 levels in BALF and EBC samples were measured with an enzyme-immunosorbent assay kit. The mean (±SEM) IL-8 concentrations in BALF and EBC were higher in SLE patients compared to healthy controls (34.84 ± 95.0 vs. 7.65 ± 21.22 pg/ml, p < 0.001; 3.82 ± 0.52 pg/m vs. 1.7 ± 1.7 pg/ml, p < 0.001, respectively). SLE patients had increased percentage of neutrophils in BALF when compared with control group (1.00 ± 5.99 vs. 0.00 ± 0.56 %, p = 0.0003). Pulmonary fibrosis in HRCT was found in 50 % of SLE patients. The disease activity scored by SLAM was significantly higher and total lung capacity was significantly lower in SLE patients with pulmonary fibrosis (8.00 ± 3.17 vs. 6.00 ± 2.31, p = 0.01; 88.00 ± 28.29 vs. 112.00 ± 21.08 % predicted, p = 0.01, respectively). In SLE patients with pulmonary fibrosis, correlations were found between SLAM and IL-8 concentration in BALF, forced expiratory volume in 1 s and forced vital capacity (r = 0.65, p = 0.006; r = -0.53, p = 0.035; r = -0.67, p = 0.006, respectively). Our results indicate that IL-8 plays an important role in the pathogenesis of SLE. An increased concentration of IL-8 according to BALF could be considered as a useful biomarker of SLE activity and pulmonary fibrosis in SLE.

Exhaled cytokines in systemic lupus erythematosus with lung involvement.

INTRODUCTION: An inflammatory process in systemic lupus erythematosus (SLE) affects many organs including the lungs. Interleukin (IL) 6 and IL­10 are suggested to play an important role in the pathogenesis of SLE. OBJECTIVES: The aim of the study was to evaluate IL­6 and IL­10 levels in the exhaled breath condensate (EBC) and bronchoalveolar lavage fluid (BALF) of patients with and without pulmonary involvement in SLE. PATIENTS AND METHODS: The study included 34 patients with SLE and 31 healthy controls evaluated using high-resolution computed tomography, pulmonary function tests, the Systemic Lupus Activity Measure (SLAM), and IL-6 and IL-10 measurement (by an enzyme­linked immunosorbent assay) in the BALF and EBC. RESULTS: The mean IL­6 and IL­10 concentrations in the BALF and the IL­10 concentration in the EBC were higher in patients with SLE compared with healthy controls (4.03 ±8.3 vs. 0.62 ±1.2 pg/ml, P <0.0001; 5.54 ±1.85 vs. 0.00 ±1.82 pg/ml, P <0.0001; 8.28 ±2.7 vs. 0.00 ±1.68 pg/ml, P <0.0001, respectively). The IL­10 level in the EBC correlated with SLE activity (r = -0.40, P = 0.019). The SLAM was significantly higher and the total lung capacity was significantly lower in patients with pulmonary manifestation of SLE compared with those without such complications (8.00 ±3.17 vs. 6.00 ±2.31, P = 0.01; 88.00 ±28.29 vs. 112 ±21.08 % predicted, P = 0.01; respectively). In patients with pulmonary involvement, correlations were observed between the IL­10 level in the EBC and the percentage of lymphocytes in the BALF (r = -0.5, P = 0.04). CONCLUSIONS: Our results indicate that IL­6 and IL­10 are involved in the pathogenesis of SLE. The measurement of IL­10 in the EBC may be a useful biomarker of SLE activity. It is likely that IL­10 protects against pulmonary manifestations of SLE.

[Etiologic agents of pneumonia and the relation to the radiographic findings]. / Patogeny a obraz radiologiczny pozaszpitalnego zapalenia pluc.

INTRODUCTION: The aim of this study was to asses correlation between etiological causative agents of community-acquired pneumonia and localization of inflammatory focuses in the lung. MATERIALS AND METHODS: Samples of sputum, bronchoaspirate and BAL's from 62 patients hospitalized due to community-acquired pneumonia were microbiological tested. Chest radiographs of patients were analyzed. RESULTS: Streptococcus pneumoniae caused inflammatory focuses more frequent in the lower right part of the lung. Gram-negative rods were more frequent cause of inflammatory focuses localized in the lower left side of the lung. Streptococcus pneumoniae more frequent caused inflammation one lobe of the lung and Gram-negative rods more than one part of the lung. CONCLUSIONS: Results of this study confirm correlation between isolated pathogen, localization of the inflammatory response in the lung in patients with community-acquired pneumonia.