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Dezfoli NK, Alipour SD, Khosravi AA, et al., 2018, Association of Pre-miR-rs2910164 polymorphism with non-small cell lung cancer in an Iranian population, 28th International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Yao X, Jia M, Yan X, et al., 2018, Ezrin, a membrane cytoskeleton cross linker protein, as a marker of epithelial damage in asthma, 28th International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Mullegama R, Pavlidis S, Chung KF, et al., 2018, Clinical and transcriptomic profiles of severe asthmatics with high or low expression of the glucocorticoid receptor and importin-7., 28th International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
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Mortaz E, Asef A, Ghaffaripour H, et al., 2018, Association of HLA-DR alleles with pulmonary cystic fibrosis, 28th International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Bozier J, Xenaki D, Adcock I, et al., 2018, Lung cells from people with COPD are hyperresponsive to E-cigarette vapour, 28th International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Allam VSRR, Adcock I, Chung KF, et al., 2018, MIF antagonism restores corticosteroid sensitivity in a murine model of severe asthma, 28th International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Shaw D, Bansal AT, Riley J, et al., 2018, Late Breaking Abstract - Longitudinal analysis of variation in clinical features from the U-BIOPRED severe asthma cohort, 28th International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Tregoning JS, Mallia P, Webber J, et al., 2018, Role of airway glucose in bacterial infections in chronic obstructive pulmonary disease, Journal of Allergy and Clinical Immunology, Vol: 142, Pages: 815-823.e6, ISSN: 0091-6749
BackgroundPatients with chronic obstructive pulmonary disease (COPD) have increased susceptibility to respiratory tract infection, which contributes to disease progression and mortality, but mechanisms of increased susceptibility to infection remain unclear.ObjectivesThe aim of this study was to determine whether glucose concentrations were increased in airway samples (nasal lavage fluid, sputum, and bronchoalveolar lavage fluid) from patients with stable COPD and to determine the effects of viral infection on sputum glucose concentrations and how airway glucose concentrations relate to bacterial infection.MethodsWe measured glucose concentrations in airway samples collected from patients with stable COPD and smokers and nonsmokers with normal lung function. Glucose concentrations were measured in patients with experimentally induced COPD exacerbations, and these results were validated in patients with naturally acquired COPD exacerbations. Relationships between sputum glucose concentrations, inflammatory markers, and bacterial load were examined.ResultsSputum glucose concentrations were significantly higher in patients with stable COPD compared with those in control subjects without COPD. In both experimental virus-induced and naturally acquired COPD exacerbations, sputum and nasal lavage fluid glucose concentrations were increased over baseline values. There were significant correlations between sputum glucose concentrations and sputum inflammatory markers, viral load, and bacterial load. Airway samples with higher glucose concentrations supported more Pseudomonas aeruginosa growth in vitro.ConclusionsAirway glucose concentrations are increased in patients with stable COPD and further increased during COPD exacerbations. Increased airway glucose concentrations might contribute to bacterial infections in both patients with stable and those with exacerbated COPD. This has important implications for the development of nonantibiotic therapeutic strategies for the prev
Kiani A, Adcock IM, Taghavi K, et al., 2018, CD4:CD8 ratio: A valuable diagnostic parameter for pulmonary sarcoidosis, Acta Facultatis Medicae Naissensis, Vol: 35, Pages: 216-225, ISSN: 0351-6083
Sarcoidosis is a multi-organ disease and is characterized by sarcoidal noncaseating granuloma comprised of T-helper/inducer (CD4+) lymphocytes and scant cytotoxic (CD8+) T-lymphocytes. CD4+:CD8+ T-cell elevated ratio is a characteristic diagnostic parameter for sarcoidosis. This is the first report from Iran evaluating the CD4:CD8 ratio capability in differentiating pulmonary sarcoidosis from other interstitial lung diseases (ILDs) on a large cohort. Fifty pulmonary sarcoidosis patients and 50 non-sarcoidosis interstitial lung diseases (nsILDs) patients were included in the current study. Bronchoalveolar lavage (BAL) was performed using flexible fiberoptic bronchoscopy and flow cytometer. Non-sarcoidosis group was established by 50 components that were classified into eight subgroups. Fifty-two percent of sarcoidosis patients and 62% of non-sarcoidosis interstitial lung disease patients had normal spirometric results. The CD4/CD8 ratio was significantly higher in sarcoidosis than in non-sarcoidosis interstitial lung diseases (p < 0.001). The CD4/CD8 ratio was found to be > 3.5 in 33.3%, 2.5-3.5 in 7.1%, 1.5-2.5 in 20.2% and < 1.5 in 39.4% of the entire study population. The best cut off point was 1.1 with the sensitivity of 92% and specificity of 80% for distinguishing sarcoidosis from other interstitial lung diseases. Performing bronchoalveolar lavage as the safe and rapid first step confirms the diagnosis of sarcoidosis in 92% of cases (current study sensitivity). Hence, performing an invasive procedure was required in a few patients only. Bronchoalveolar lavage flow cytometry in the assessment of clinical and radiological findings supplies an appropriate diagnostic adjunct for discriminating sarcoidosis from non-sarcoidosis interstitial lung diseases.
Maneechotesuwan K, Yao X, Ito K, et al., 2018, Correction: Suppression of GATA-3 nuclear import and phosphorylation: a novel mechanism of corticosteroid action in allergic disease, PLoS Medicine, Vol: 15, ISSN: 1549-1277
[This corrects the article DOI: 10.1371/journal.pmed.1000076.].
Mazein A, Knowles RG, Adcock I, et al., 2018, AsthmaMap: An expert-driven computational representation of disease mechanisms, Clinical and Experimental Allergy, Vol: 48, Pages: 916-918, ISSN: 0954-7894
Alipoor SD, Mortaz E, Tabarsi P, et al., 2018, miR-1224 Expression Is Increased in Human Macrophages after Infection with Bacillus Calmette-Guerin (BCG), IRANIAN JOURNAL OF ALLERGY ASTHMA AND IMMUNOLOGY, Vol: 17, Pages: 250-257, ISSN: 1735-1502
Understanding the strategies mycobacteria take to overcome immune defense is important in order to control the infection. Micro (mi)RNAs are master regulators of most pathways in the human body. Infection with mycobacterium impacts upon the host metabolic pathways as they are subverted to obtain the nutrition for intracellular TB survival. In this study, we aimed to investigate the effect of Bacillus Calmette-Guérin (BCG) infection on the expression of three miRNAs (miR-1224, -484 and -425), which are important in infection and in the regulation of metabolic pathways. Peripheral blood monocyte-derived macrophage (MDM) cultures were prepared and infected with BCG at a multiplicity of infection (MOI)=10 or left uninfected as a control. 72h post-infection, RNA was extracted from the cultured cells and cDNA synthesis and real-time PCR performed. Expression levels miRNAs were normalized to the levels of U6 snRNA (Rnu6) using the 2–ΔΔCt method. Infection with BCG resulted in a highly significant increase in miR-1224 expression (24.4±3.8-fold induction) in human MDMs. The induction of miR-484 (1.8±0.3-fold increase) and of miR-425 (1.2±0.2-fold increase) was less increased compared to miR-1224. Mycobacterium tolerates a hostile microenvironment by escaping from lysosomal degradation and providing a lipid-rich niche by trigger with and re-pattering host metabolism. This study highlighted the potential roles of miRNAs in host responses upon mycobacterium infection.
Burg D, Schofield JPR, Brandsma J, et al., 2018, Large-scale label-free quantitative mapping of the sputum proteome, Journal of Proteome Research, Vol: 17, Pages: 2072-2091, ISSN: 1535-3893
Analysis of induced sputum supernatant is a minimally invasive approach to study the epithelial lining fluid and, thereby, provide insight into normal lung biology and the pathobiology of lung diseases. We present here a novel proteomics approach to sputum analysis developed within the U-BIOPRED (unbiased biomarkers predictive of respiratory disease outcomes) international project. We present practical and analytical techniques to optimize the detection of robust biomarkers in proteomic studies. The normal sputum proteome was derived using data-independent HDMSE applied to 40 healthy nonsmoking participants, which provides an essential baseline from which to compare modulation of protein expression in respiratory diseases. The "core" sputum proteome (proteins detected in ≥40% of participants) was composed of 284 proteins, and the extended proteome (proteins detected in ≥3 participants) contained 1666 proteins. Quality control procedures were developed to optimize the accuracy and consistency of measurement of sputum proteins and analyze the distribution of sputum proteins in the healthy population. The analysis showed that quantitation of proteins by HDMSE is influenced by several factors, with some proteins being measured in all participants' samples and with low measurement variance between samples from the same patient. The measurement of some proteins is highly variable between repeat analyses, susceptible to sample processing effects, or difficult to accurately quantify by mass spectrometry. Other proteins show high interindividual variance. We also highlight that the sputum proteome of healthy individuals is related to sputum neutrophil levels, but not gender or allergic sensitization. We illustrate the importance of design and interpretation of disease biomarker studies considering such protein population and technical measurement variance.
Caramori G, Ruggeri P, Di Stefano A, et al., 2018, Autoimmunity and COPD: clinical implications, Chest, Vol: 153, Pages: 1424-1431, ISSN: 0012-3692
Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. Long term cigarette smoking is the cause of more than 90% of COPD in Westernized countries. However, only a fraction of chronic heavy smokers develop symptomatic COPD by the age of 80 years. COPD is characterized by an abnormal immune response in the lower airways and its progression is associated with infiltration of the lung by innate and adaptive inflammatory immune cells that form lymphoid follicles. There is growing evidence that both cellular- and antibody-mediated autoimmunity has a fundamental role in the pathogenesis of stable COPD. In particular, carbonyl-modified proteins may help to drive autoimmunity in COPD and to cause the characteristic small airways abnormalities and even contribute to the pathogenesis of pulmonary emphysema. Although direct, indirect, and circumstantial evidence of a role for autoimmunity in stable COPD patients has been identified, no cause-and-effect relationship between autoimmunity and the mechanisms of COPD has been firmly established in man. As such the potential contribution of an autoimmune response to the pathogenesis of COPD exacerbation is still being investigated and represents an area of active research. Many drugs targeting autoimmune responses are already available and the results of controlled clinical trials are awaited with great interest. The potential for measuring specific serum autoantibodies as biomarkers to predict clinical phenotypes or progression of stable COPD is promising.
Alinejad Dizaj M, Mortaz E, Mahdaviani SA, et al., 2018, Susceptibility to mycobacterial disease due to mutations in IL-12Rβ1 in three Iranian patients, Immunogenetics, Vol: 70, Pages: 373-379, ISSN: 0093-7711
In the last decade, autosomal recessive interleukin-12 receptor β1 (IL-12Rβ1) deficiency, the most common cause of Mendelian susceptibility to mycobacterial disease (MSMD), has been diagnosed in a few children and adults with severe tuberculosis in Iran. Here, we report three cases referred to the Immunology, Asthma and Allergy ward at the National Research Institute of Tuberculosis and Lung Diseases (NRITLD) at Masih Daneshvari Hospital from 2012 to 2017 with Mycobacterium tuberculosis and non-tuberculous mycobacteria infections due to defects in IL-12Rβ1 but with different clinical manifestations. All three were homozygous for either an IL-12Rβ1 missense or nonsense mutation that caused the IL-12Rβ1 protein not to be expressed on the cell membrane and completely abolished the cellular response to recombinant IL-12. Our findings suggest that the presence of IL-12Rβ1 deficiency should be determined in children with mycobacterial infections at least in countries with a high prevalence of parental consanguinity and in areas endemic for TB like Iran.
De Meulder B, Lefaudeux D, Bansal AT, et al., 2018, A computational framework for complex disease stratification from multiple large-scale datasets, BMC Systems Biology, Vol: 12, ISSN: 1752-0509
BACKGROUND: Multilevel data integration is becoming a major area of research in systems biology. Within this area, multi-'omics datasets on complex diseases are becoming more readily available and there is a need to set standards and good practices for integrated analysis of biological, clinical and environmental data. We present a framework to plan and generate single and multi-'omics signatures of disease states. METHODS: The framework is divided into four major steps: dataset subsetting, feature filtering, 'omics-based clustering and biomarker identification. RESULTS: We illustrate the usefulness of this framework by identifying potential patient clusters based on integrated multi-'omics signatures in a publicly available ovarian cystadenocarcinoma dataset. The analysis generated a higher number of stable and clinically relevant clusters than previously reported, and enabled the generation of predictive models of patient outcomes. CONCLUSIONS: This framework will help health researchers plan and perform multi-'omics big data analyses to generate hypotheses and make sense of their rich, diverse and ever growing datasets, to enable implementation of translational P4 medicine.
Alavi-Moghaddam M, Chehrazi M, Alipoor SD, et al., 2018, A preliminary study of microRNA-208b after acute myocardial infarction: impact on 6-months survival, Disease Markers, ISSN: 0278-0240
miRNAs contribute to a variety of essential biological processes including development, proliferation, differentiation, and apoptosis. Circulating microRNAs are very stable and have shown potential as biomarkers of cardiovascular disease. microRNA-208b expression was increased in the blood of patients with acute myocardial infarction (AMI) and has been proposed as a biomarker for early diagnosis. In this pilot study, we investigate the potential of circulating miR-208b as a prognostic biomarker of 6-month survival in AMI patients. Methods. Plasma samples from 21 patients and 8 age- and gender-matched healthy adults were collected, and circulating levels of miR-208b were detected using quantitative real-time PCR. Results. miR-208b levels were higher in healthy control subjects (9.6-fold; ). Within the AMI patients, the levels of miR-208b were significantly lower in the survivor versus nonsurvivor group (fold change = 6.51 and 14.1, resp.; ). The Kaplan-Meier curve revealed that the 6-month survival time was significantly higher among AMI patients with a relative expression of miR-208b lower than 12.38. The hazard ratio (HR) for the relative expression of miR-208b (<12.38 was the reference) was 5.08 (95% CI: 1.13–22.82; ). Conclusion. Our results showed that elevated miR-208b expression was associated with reduced long-term survival in AMI patients. These pilot data indicate the need for a large follow-up study to confirm whether miR-208b can be used as a predictor of 6-month survival time after AMI.
Perry MM, Tildy B, Papi A, et al., 2018, The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide., Respiratory Research, Vol: 19, ISSN: 1465-9921
BACKBROUND: COPD is a common, highly debilitating disease of the airways, primarily caused by smoking. Chronic inflammation and structural remodelling are key pathological features of this disease caused, in part, by the aberrant function of airway smooth muscle (ASM). We have previously demonstrated that hydrogen sulfide (H2S) can inhibit ASM cell proliferation and CXCL8 release, from cells isolated from non-smokers. METHODS: We examined the effect of H2S upon ASM cells from COPD patients. ASM cells were isolated from non-smokers, smokers and patients with COPD (n = 9). Proliferation and cytokine release (IL-6 and CXCL8) of ASM was induced by FCS, and measured by bromodeoxyuridine incorporation and ELISA, respectively. RESULTS: Exposure of ASM to H2S donors inhibited FCS-induced proliferation and cytokine release, but was less effective upon COPD ASM cells compared to the non-smokers and smokers. The mRNA and protein expression of the enzymes responsible for endogenous H2S production (cystathionine-β-synthase [CBS] and 3-mercaptopyruvate sulphur transferase [MPST]) were inhibited by H2S donors. Finally, we report that exogenous H2S inhibited FCS-stimulated phosphorylation of ERK-1/2 and p38 mitogen activated protein kinases (MAPKs), in the non-smoker and smoker ASM cells, with little effect in COPD cells. CONCLUSIONS: H2S production provides a novel mechanism for the repression of ASM proliferation and cytokine release. The ability of COPD ASM cells to respond to H2S is attenuated in COPD ASM cells despite the presence of the enzymes responsible for H2S production.
Mortaz E, Alipoor SD, Varahram M, et al., 2018, Exosomes in Severe Asthma: Update in Their Roles and Potential in Therapy, BIOMED RESEARCH INTERNATIONAL, Vol: 2018, ISSN: 2314-6133
Exosomes are nanosized vesicles and have recently been recognized as important players in cell-to-cell communication. Exosomes contain different mediators such as proteins, nucleic acids (DNA, mRNA, miRNAs, and other ncRNAs), and lipid mediators and can shuttle their exosomal content to both neighboring and distal cells. Exosomes are very effective in orchestrating immune responses in the airways and all cell types can contribute to the systemic exosome pool. Intracellular communication between the broad range of cell types within the lung is crucial in disease emphasizing the importance of exosomes. In asthma, exosomes affect the inflammatory microenvironment which ultimately determines the development or alleviation of the pathological symptoms. Recent studies in this area have provided insight into the underlying mechanisms of disease and led to interest in using exosomes as potential novel therapeutic agents.
Takahashi K, Pavlidis S, Ng Kee Kwong F, et al., 2018, Sputum proteomics and airway cell transcripts of current and ex-smokers with severe asthma in U-BIOPRED: an exploratory analysis, European Respiratory Journal, Vol: 51, ISSN: 0903-1936
Background: Severe asthma patients with a significant smoking history have airflow obstruction with reported neutrophilia. We hypothesise that multi1omic analysis will enable the definition of smoking and ex1smoking severe asthma molecular phenotypes.Methods The U1BIOPRED severe asthma patients containing current1smokers (CSA), ex1smokers (ESA), non1smokers (NSA) and healthy non1smokers (NH) was examined. Blood and sputum cell counts, fractional exhaled nitric oxide and spirometry were obtained. Exploratory proteomic analysis of sputum supernatants and transcriptomic analysis of bronchial brushings, biopsies and sputum cells was performed. Results Colony stimulating factor (CSF)2 protein levels were increased in CSA sputum supernatants with azurocidin 1, neutrophil elastase and CXCL8 upregulated in ESA. Phagocytosis and innate immune pathways were associated with neutrophilic inflammation in ESA. Gene Set Variation Analysis of bronchial epithelial cell transcriptome from CSA showed enrichment of xenobiotic metabolism, oxidative stress and endoplasmic reticulum stress compared to other groups. CXCL5 and matrix metallopeptidase 12 genes were upregulated in ESA and the epithelial protective genes, mucin 2 and cystatin SN, were downregulated. Conclusion Despite little difference in clinical characteristics, CSA were distinguishable from ESA subjects at the sputum proteomic level with CSA having increased CSF2 expression and ESA patients showed sustained loss of epithelial barrier processes.
Mortaz E, Garssen J, Roos D, et al., 2018, Unusual fungal infection in adults chronic granulomatous diseases, 2018 CIS Annual Meeting: Immune Deficiency & Dysregulation North American Conference, Publisher: SPRINGER/PLENUM PUBLISHERS, Pages: 413-414, ISSN: 0271-9142
Perry M, Tildy B, Papi A, et al., 2018, The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle, Respiratory Research, ISSN: 1465-9921
Backbround: COPD is a common, highly debilitating disease of the airways, primarily caused49 by smoking. Chronic inflammation and structural remodelling are key pathological features of50 this disease caused, in part, by the aberrant function of airway smooth muscle (ASM). We have1234567891011121314151617181920212223242526272829303132333435363738394041424344454647484950515253545556575859606162636465previously demonstrated that hydrogen sulfide (H2S) 51 can inhibit ASM cell proliferation and52 CXCL8 release, from cells isolated from non-smokers.53 Methods: We examined the effect of H2S upon ASM cells from COPD patients. ASM cells54 were isolated from non-smokers, smokers and patients with COPD (n = 9). Proliferation and55 cytokine release (IL-6 and CXCL8) of ASM was induced by FCS, and measured by56 bromodeoxyuridine incorporation and ELISA, respectively.57 Results: Exposure of ASM to H2S donors inhibited FCS-induced proliferation and cytokine58 release, but was less effective upon COPD ASM cells compared to the non-smokers and59 smokers. The mRNA and protein expression of the enzymes responsible for endogenous H2S60 production (cystathionine-β-synthase [CBS] and 3-mercaptopyruvate sulphur transferase61 [MPST]) were inhibited by H2S donors. Finally, we report that exogenous H2S inhibited FCS62stimulated phosphorylation of ERK–1/2 and p38 mitogen activated protein kinases (MAPKs),63 in the non-smoker and smoker ASM cells, with little effect in COPD cells.64 Conclusions: H2S production provides a novel mechanism for the repression of ASM65 proliferation and cytokine release. The ability of COPD ASM cells to respond to H2S is66 attenuated in COPD ASM cells despite the presence of the enzymes responsible for H2S67 production.68
Alipoor SD, Mortaz E, Varahram M, et al., 2018, The Potential Biomarkers and Immunological Effects of Tumor-Derived Exosomes in Lung Cancer, FRONTIERS IN IMMUNOLOGY, Vol: 9, ISSN: 1664-3224
Lung cancer remains the leading cause of cancer-related deaths worldwide. Despite considerable achievements in lung cancer diagnosis and treatment, the global control of the disease remains problematic. In this respect, greater understanding of the disease pathology is crucially needed for earlier diagnosis and more successful treatment to be achieved. Exosomes are nano-sized particles secreted from most cells, which allow cross talk between cells and their surrounding environment via transferring their cargo. Tumor cells, just like normal cells, also secrete exosomes that are termed Tumor-Derived Exosome or tumor-derived exosome (TEX). TEXs have gained attention for their immuno-modulatory activities, which strongly affect the tumor microenvironment and antitumor immune responses. The immunological activity of TEX influences both the innate and adaptive immune systems including natural killer cell activity and regulatory T-cell maturation as well as numerous anti-inflammatory responses. In the context of lung cancer, TEXs have been studied in order to better understand the mechanisms underlying tumor metastasis and progression. As such, TEX has the potential to act both as a biomarker for lung cancer diagnosis as well as the response to therapy.
Perry MM, Lavender P, Scott Kuo C-H, et al., 2018, DNA methylation modules in airway smooth muscle are associated with asthma severity, European Respiratory Journal, Vol: 51, ISSN: 0903-1936
Abnormal DNA methylation patterns distinguish airway smooth muscle cell function in asthma and asthma severity.
Mortaz E, Moloudizargari M, Varahram M, et al., 2018, What Immunological Defects Predispose to Non-tuberculosis Mycobacterial Infections?, Iranian Journal Of Allergy, Asthma and Immunology, Vol: 17, Pages: 100-109, ISSN: 1735-1502
Nontuberculous mycobacteria (NTM) are categorized as one of the large and diverse groups of environmental organisms which are abundant in water and soil. NTM cause a variety of diseases in humans that mainly affect the lung. A predisposition to pulmonary NTM is evident in patients with parenchymal structural diseases including bronchiectasis, emphysema, tuberculosis (TB), cystic fibrosis (CF), rheumatologic lung diseases and other chronic diseases with pulmonary manifestations. Lung infections are not the only consequences of being infected by NTM as they can also infect skin and soft tissue and may also cause lymphadenitis (predominantly in young children) and disseminated disease in human immunodeficiency virus (HIV)-infected patients or those with severely compromised immune system. NTM are also found in many subjects without any known risk factors. Although the recent advances in imaging and microbiologic techniques including gene sequencing have provided a better view of the problems caused by NTM and has enhanced our understanding of the disease, many uncertainties regarding the immunologic response to NTM still exist. There is also limited data on the immunogenetics of NTM infection. Here, the authors reviewed the main immunogenetic defects as well as other immunological conditions which are associated with an increased the risk of NTM infections.
Hashemian SM, Mortaz E, Jamaati H, et al., 2018, Budesonide facilitates weaning from mechanical ventilation in difficult-to-wean very severe COPD patients: association with inflammatory mediators and cells, Journal of Critical Care, Vol: 44, Pages: 161-167, ISSN: 0883-9441
INTRODUCTION: Mechanical ventilatory support is life-saving therapy for patients with respiratory failure in intensive care units (ICU) but is linked to ventilator-associated pneumonia and other nosocomial infections. Interventions that improve the efficiency of weaning from mechanical ventilation may improve patient outcomes. OBJECTIVE: To determine whether inhaled budesonide decreases time-to-weaning in COPD stage 4 difficult-to-wean patients and reduces the release of pro-inflammatory cytokines in ICU patients. MATERIALS AND METHODS: We recruited 55 difficult-to-wean COPD patients (Stage 4) within the ICU of the Masih Daneshvari Hospital. Subjects were randomly assigned to receive inhaled budesonide (0.5mg/day) or placebo (normal saline). Dynamic compliance and BAL cytokines were measured. RESULTS: Budesonide significantly reduced the number of days on MV (days-to-weaning=4.6±1.6days) compared to that seen in the control group (7.2±2.7days, p=0.014). Dynamic compliance was significantly improved in the budesonide group on days 3 (p=0.018) and 5 (p=0.011) The levels of CXCL-8 and IL-6 diminished on days 3-5 after start of budesonide (p<0.05). CONCLUSION: In COPD patients on MV, nebulized budesonide was associated with reduced BAL CXCL8 and IL-6 levels and neutrophil numbers as well as an improvement in ventilatory mechanics and facilitated weaning.
Kiani A, Abedini A, Adcock IM, et al., 2018, Association between vitamin d deficiencies in sarcoidosis with disease activity, course of disease and stages of lung involvements, Journal of Medical Biochemistry, Vol: 37, Pages: 103-109, ISSN: 1452-8258
Background: Despite negative association between 25-hydroxy vitamin D and incidence of many chronic respiratory diseases, this feature was not well studied in sarcoidosis. Current study investigated the association between 25-hydroxy vitamin D deficiency with sarcoidosis chronicity, disease activity, extra-pulmonary skin manifestations, urine calcium level and pulmonary function status in Iranian sarcoidosis patients. Results of this study along with future studies, will supply more effective programs for sarcoidosis treatment.Methods: Eighty sarcoidosis patients in two groups of insufficient serum level and sufficient serum level of 25-hydroxy vitamin D were studied. Course of sarcoidosis was defined as acute and chronic sarcoidosis. Pulmonary function test (PFT) was assessed by spirometry. Skin involvements were defined as biopsy proven skin sarcoidosis. 24-hour urine calcium level was used to specify the disease activity. Stages of lung involvements were obtained by CT-scan and chest X-ray. The statistical analyses were evaluated using Statistical Package for the Social Sciences.Results: A significant negative correlation was obtained between vitamin D deficiency in sarcoidosis patients and disease chronic course and stages two to four of lung involvements. Considering other parameters of the disease and vitamin D deficiency, no significant correlation was detected.Conclusions: In conclusion, results of the current study implies in the role of vitamin 25(OH)D deficiencies in predicting the course of chronic sarcoidosis. Furthermore, it was concluded that vitamin 25(OH)D deficiency can direct pulmonary sarcoidosis toward stage 2–4 of lung involvements.
Taghavi M, Mortaz E, Khosravi A, et al., 2018, Zymosan attenuates melanoma growth progression, increases splenocyte proliferation and induces TLR2 and TNF-α expression in mice, Journal of inflammation, Vol: 15, ISSN: 1078-7852
Background:Melanoma is one of the most common types of skin malignancies. Since current therapies are suboptimal, considerable interest has focused on novel natural-based treatments. Toll-like receptors (TLRs) play an important role in evoking innate immunity against cancer cells. Zymosan, a known TLR-2 agonist, is a glucan derived from yeast cell walls with promising immunomodulatory effects. The aim of this study was to evaluate whether Saccharomyces cerevisiae-derived zymosan-modulated skin melanoma progression byregulation ofTLR-2 expression in peritoneal macrophages and serum TNF-level.Methods: Male C57BL/6 mice were divided into four groups: i) zymosan-treated (Z), ii) Melanoma-bearing mice (M), iii) Melanoma-bearing mice treated with zymosan (ZM) and iv) ahealthy control group (negative control). 15 days after melanoma induction, mice were injected i.p. with zymosan (10g) daily for 4 consecutive days. Mice were CO2-euthanized and serum TNF-α level, TLR-2expression in peritoneal macrophages and tumor growth measured. Splenocytes were treated ex-vivo with zymosan to determine viability and proliferation.Results:Tumor weight significantly decreased following therapeutic dosing with zymosan (P<0.05). This was associated with zymosan-induced upregulation ofTLR-2 and TNF-mRNA in peritoneal macrophages and enhanced serum TNF-levels (P<0.05). Splenocyte number and viability were increased in a concentration-dependent manner by zymosan.Conclusions:Our study suggests that zymosan-induced upregulation of TLR-2 and TNF-gene expression and ofTNF-release;together with increased levelsof lymphocyte proliferation may play a role in theinhibition of melanoma progression.
Andersson C, Bonvini SJ, Horvath P, et al., 2018, Research highlights from the 2017 ERS International Congress: airway diseases in focus, ERJ Open Research, Vol: 4, ISSN: 2312-0541
For another year, high-quality research studies from around the world transformed the annual ERS International Congress into a vivid platform to discuss trending research topics, to produce new research questions and to further push the boundaries of respiratory medicine and science. This article reviews only some of the high-quality research studies on asthma, chronic obstructive pulmonary disease (COPD), bronchiectasis and chronic cough that were presented during the congress through the Airway Diseases Assembly (ERS Assembly 5) and places them into the context of current knowledge and research challenges.
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