Increased expression of CCL4/MIP-1β in CD8+ cells and CD4+ cells in sarcoidosis.

Sarcoidosis is a granulomatous disease with an increased accumulation of T cells in lungs as a result of on-site proliferation and chemotaxis induced by chemokines. It has already been demonstrated that CCL3-5 levels were increased in BAL fluid of sarcoidosis patients. To analyze the expression of CCL3-5 chemokines by T-cell subtypes (CD4+, CD8+, Th1, Th2, Tc1 or Tc2) in the lungs of sarcoidosis patients, fifteen untreated sarcoidosis patients and eighteen control subjects were enrolled in this study. CD4+and CD8+cells were isolated from BAL fluid by positive magnetic selection. The expression of CCL3-5 and other cytokines in CD4+and CD8+cells were measured by flow cytometry. The percentage of CD4+or CD8+cells expressing CCL4 were significantly higher in sarcoidosis patients (22.3% and 58.1%) compared to those seen in healthy subjects (11.1% and 16.5%, P = 0.04 and P = 0.02, respectively). In addition, the expression of CCL3, CCL4 and CCL5 was significantly elevated in CD8+cells (8.9%, 58.1% and 2.1%) compared to CD4+cells (2.1%, 22.3% and 0.7%; P = 0.04, P = 0.009 and P = 0.04, respectively), whereas CCL4 was expressed by significantly more Tc1 than Th1 cells in sarcoidosis patients (P = 0.006). Our study shows the possible role of CD8+cells and CD4+cells in recruiting T cells to the site of inflammation in sarcoidosis through the release of CCL4, either alone or together with Th1/Tc1-associated cytokines

Fluticasone furoate and vilanterol for the treatment of chronic obstructive pulmonary disease

Introduction: Current national and international guidelines for the management of patients with stable chronic obstructive pulmonary disease (COPD) recommend the use of inhaled long-acting bronchodilators, inhaled glucocorticoids and their combinations for maintenance treatment of moderate to severe stable COPD. Areas covered: The role of fluticasone furoate (FF) and vilanterol (VI) once daily combination therapy for the regular treatment of patients with stable COPD is discussed in this review. Expert commentary: The regular treatment of moderate to severe stable COPD with once daily FF/VI combination therapy is effective, as seen in in several large placebo-controlled clinical trials involving many thousands of patients. FF/VI improved lung function, decreased respiratory symptoms and deceased the number of COPD exacerbations, including COPD-related hospitalizations. FF/VI combination therapy has also been approved for this indication in most countries. The use of this combination therapy may significantly decrease the economic costs for some National Health Services

Indicadores biofísicos de sistemas agroflorestais.

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High resolution computed tomography quantitation of emphysema is correlated with selected lung function values in stable COPD.

BACKGROUND: The literature shows conflicting results when high-resolution computed tomography (HRCT) scores of emphysema were correlated with different indices of airflow obstruction. OBJECTIVES: We correlated HRCT scores of emphysema with different indices of airflow obstruction. METHODS: We performed HRCT of the chest in 59 patients, all smokers or ex-smokers, with stable chronic obstructive pulmonary disease of different severity [GOLD stages I-IV; mean age \ub1 SD 67.8 \ub1 7.3 years; pack/years 51.0 \ub1 34.6; percent predicted forced expiratory volume in 1 s (FEV(1)% predicted) 52.3 \ub1 17.6; post-bronchodilator FEV(1)% predicted 56.5 \ub1 19.1; FEV(1)/forced vital capacity (FVC) ratio 50.8 \ub1 10.2; post-bronchodilator FEV(1)/FVC ratio 51.6 \ub1 11.0; percent diffusion lung capacity for carbon monoxide (DLCO%) 59.2 \ub1 21.1; DLCO/percent alveolar volume (VA%) 54.5 \ub1 18.2; percent residual volume 163.0 \ub1 35.6; percent total lung capacity (TLC%) 113.2 \ub1 15; residual volume/TLC 1.44 \ub1 0.2]. All patients were in stable phase. RESULTS: The mean \ub1 SD visual emphysema score in all patients was 25.6 \ub1 25.4%. There was a weak but significant correlation between the percentage of pulmonary emphysema and numbers of pack/years (R = +0.31, p = 0.024). The percentage of emphysema was inversely correlated with the FEV(1)/FVC ratio before and after bronchodilator use (R = -0.44, p = 0.002, and R = -0.39, p = 0.005), DLCO% (R = -0.64, p = 0.0003) and DLCO/VA% (R = -0.68, p < 0.0001). A weak positive correlation was also found with TLC% (R = +0.28, p = 0.048). When patients with documented emphysema were considered separately, the best significant correlation observed was between DLCO/VA% and HRCT scan score (p = 0.007). CONCLUSIONS: These data suggest that in patients with stable chronic obstructive pulmonary disease of varying severity, the presence of pulmonary emphysema is best represented by the impaired gas exchange capability of the respiratory system

Photoelectrochemical Valorization of Biomass Derivatives with Hematite Photoanodes Modified by Cocatalysts

The solar-driven oxidation of biomass to valuable chemicals is rising as a promising anodic reaction in photoelectrochemical cells, replacing the sluggish oxygen evolution reaction and improving the added value of the energy conversion process. Herein, the photooxidation of 5-hydroxymethylfurfural into furan dicarboxylic acid (FDCA) is performed in basic aqueous environment (borate buffer, pH 9.2), with the addition of 2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPO) as redox mediator. Because of its good stability, cost-effectiveness, and nontoxicity, titanium-modified hematite (Ti:Fe2O3) photoanodes are investigated to this aim, and their performance is tuned by engineering the semiconductor surface with a thin layer of Co-based cocatalysts, i.e., cobalt iron oxide (CoFeO x ) and cobalt phosphate (CoPi). Interestingly, the electrode modified with CoPi shows improved efficiency and selectivity toward the final product FDCA The source of this enhancement is correlated to the effect of the cocatalyst on the charge carrier dynamics, which is investigated by electrochemical impedance spectroscopy and intensity-modulated photocurrent spectroscopy analysis. In addition, the results of the latter are interpreted through a novel approach called Lasso distribution of relaxation time, revealing that CoPi cocatalyst is effective in the suppression of the recombination processes and in the enhancement of direct hole transfer to TEMPO

Phospho-p38 MAPK expression in COPD patients and asthmatics and in challenged bronchial epithelium

Background: The role of mitogen-activated protein kinases (MAPK) in regulating the inflammatory response in the airways of patients with chronic obstructive pulmonary disease (COPD) and asthmatic patients is unclear. Objectives: To investigate the expression of activated MAPK in lungs of COPD patients and in bronchial biopsies of asthmatic patients and to study MAPK expression in bronchial epithelial cells in response to oxidative and inflammatory stimuli. Methods: Immunohistochemical expression of phospho (p)-p38 MAPK, p-JNK1 and p-ERK1/2 was measured in bronchial mucosa in patients with mild/moderate (n = 17), severe/very severe (n = 16) stable COPD, control smokers (n = 16), control non-smokers (n = 9), in mild asthma (n = 9) and in peripheral airways from COPD patients (n = 15) and control smokers (n = 15). Interleukin (IL)-8 and MAPK mRNA was measured in stimulated 16HBE cells. Results: No significant differences in p-p38 MAPK, p-JNK or p-ERK1/2 expression were seen in bronchial biopsies and peripheral airways between COPD and control subjects. Asthmatics showed increased submucosal p-p38 MAPK expression compared to COPD patients (p 2O2), cytomix (tumour necrosis factor-\u3b1 + IL-1\u3b2 + interferon-\u3b3) and lipopolysaccharide (LPS) upregulated IL-8 mRNA at 1 or 2 h. p38 MAPK\u3b1 mRNA was significantly increased after H2O2 and LPS treatment. JNK1 and ERK1 mRNA were unchanged after H2O2, cytomix or LPS treatments. Conclusion: p-p38 MAPK expression is similar in stable COPD and control subjects but increased in the bronchi of mild asthmatics compared to stable COPD patients. p38 MAPK mRNA is increased after bronchial epithelial challenges in vitro. These data together suggest a potential role for this MAPK in Th2 inflammation and possibly during COPD exacerbations

Soluble major histocompatibility complex class I-related chain B molecules are increased and correlate with clinical outcomes during rhinovirus infection in healthy subjects

BACKGROUND: Surface major histocompatibility complex class I-related chain (MIC) A and B molecules are increased by IL-15 and have a role in the activation of natural killer group 2 member D-positive natural killer and CD8 T cells. MICA and MICB also exist in soluble forms (sMICA and sMICB). Rhinoviruses (RVs) are the major cause of asthma exacerbations, and IL-15 levels are decreased in the airways of subjects with asthma. The role of MIC molecules in immune responses in the lung has not been studied. Here, we determine the relationship between MICA and MICB and RV infection in vitro in respiratory epithelial cells and in vivo in healthy subjects and subjects with asthma. METHODS: Surface MICA and MICB, as well as sMICA and sMICB, in respiratory epithelial cells were measured in vitro in response to RV infection and exposure to IL-15. Levels of sMICA and sMICB in serum, sputum, and BAL were measured and correlated with blood and bronchoalveolar immune cells in healthy subjects and subjects with asthma before and during RV infection. RESULTS: RV increased MICA and MICB in vitro in epithelial cells. Exogenous IL-15 upregulated sMICB levels in RV-infected epithelial cells. Levels of sMICB molecules in serum were increased in healthy subjects compared with subjects with stable asthma. Following RV infection, airway levels of sMIC are upregulated, and there are positive correlations between sputum MICB levels and the percentage of bronchoalveolar natural killer cells in healthy subjects but not subjects with asthma. CONCLUSIONS: RV infection induces MIC molecules in respiratory epithelial cells in vitro and in vivo. Induction of MICB molecules is impaired in subjects with asthma, suggesting these molecules may have a role in the antiviral immune response to RV infections

Bronchial glomus tumor mimicking a COPD exacerbation

We report the case of a glomus tumor originating in the left main bronchus diagnosed in a 79 year old Caucasian man. A glomus tumor is an extremely rare neoplasm in the bronchi with nonspecific clinical features. Bronchoscopy allows the diagnosis through biopsy and subsequent histopathological examination of the tissue and in selected cases may represent a valid alternative to surgery permitting a radical tumor excision

Decreased humoral immune response in the bronchi of rapid decliners with chronic obstructive pulmonary disease

Background: Identification of COPD patients with a rapid decline in FEV1 is of particular interest for prognostic and therapeutic reasons. Objective: To determine the expression of markers of inflammation in COPD patients with rapid functional decline in comparison to slow or no decliners. Methods: In COPD patients monitored for at least 3&nbsp;years (mean ± SD: 5.8 ± 3&nbsp;years) for lung functional decline, the expression and localization of inflammatory markers was measured in bronchial biopsies of patients with no lung functional decline (FEV1% + 30 ± 43&nbsp;ml/year, n = 21), slow (FEV1% ml/year, −&nbsp;40 ± 19, n = 14) and rapid decline (FEV1% ml/year, −&nbsp;112 ± 53, n = 15) using immunohistochemistry. ELISA test was used for polymeric immunoglobulin receptor (pIgR) quantitation “in vitro”. Results: The expression of secretory IgA was significantly reduced in bronchial epithelium (p = 0.011) and plasma cell numbers was significantly reduced in the bronchial lamina propria (p = 0.017) of rapid decliners compared to no decliners. Bronchial inflammatory cell infiltration, CD4, CD8, CD68, CD20, NK, neutrophils, eosinophils, mast cells, pIgR, was not changed in epithelium and lamina propria of rapid decliners compared to other groups. Plasma cells/mm2 correlated positively with scored total IgA in lamina propria of all patients. “In vitro” stimulation of 16HBE cells with LPS (10&nbsp;μg/ml) and IL-8 (10&nbsp;ng/ml) induced a significant increase while H2O2 (100&nbsp;μM) significantly decreased pIgR epithelial expression. Conclusion: These data show an impaired humoral immune response in rapid decliners with COPD, marked by reduced epithelial secretory IgA and plasma cell numbers in the bronchial lamina propria. These findings may help in the prognostic stratification and treatment of COPD