Athens Chest Hospital Sotiria

Athens, Greece

Athens Chest Hospital Sotiria

Athens, Greece
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Trochoutsou A.I.,BiomedicalResearch Foundation of the Academy of Athens | Kloukina V.,BiomedicalResearch Foundation of the Academy of Athens | Samitas K.,BiomedicalResearch Foundation of the Academy of Athens | Samitas K.,Athens Chest Hospital Sotiria | Xanthou G.,BiomedicalResearch Foundation of the Academy of Athens
Mini-Reviews in Medicinal Chemistry | Year: 2015

More than thirty years ago functions of vitamin D other than its beneficial effects on calcium homeostasis and bone metabolism have been identified, mainly in relation to its antiproliferative effects on cancer cells. Notably, vitamin D deficiency has been associated with a number of pathological conditions, including infections, autoimmune and allergic diseases. Vitamin D, and its metabolites, are actively involved in the regulation of innate and adaptive immune responses. Vitamin D signals through the vitamin D receptor (VDR), a specific zinc-finger nuclear receptor. The functions of vitamin D are characterized as genomic, mediated through the VDR transcriptional effects inside the cell nucleus, and non-genomic, when the VDR induces rapid signaling, situated on the cell membrane and/or cytoplasm. Emerging evidence supports the notion that vitamin D enhances immunity, providing protection towards pathogens, while, concomitantly, it exerts immunosuppressive effects by preventing the detrimental effects of prolonged inflammatory responses to the host. Still, the precise molecular mechanisms involved in vitamin D’s genomic and non-genomic actions remain incompletely defined. Moreover, it is unclear whether vitamin D actions require the synergistic activation of other mediators, such as nuclear membrane receptors. Understanding the biology of vitamin D and the molecular pathways utilized will pave the way for the design of more effective therapeutic strategies. In this review, we present the recent genomic and non-genomic effects of vitamin D from an immunological perspective with a focus on immune-mediated diseases. © 2015, Bentham Science Publishers.


Thiriou D.,Athens Chest Hospital Sotiria | Morianos I.,Biomedical Research Foundation of the Academy of Athens | Xanthou G.,Biomedical Research Foundation of the Academy of Athens | Samitas K.,Biomedical Research Foundation of the Academy of Athens | Samitas K.,Athens Chest Hospital Sotiria
International Immunopharmacology | Year: 2017

The respiratory system is constantly in direct contact with the environment and, has therefore, developed strong innate and adaptive immune responses to combat pathogens. Unlike adaptive immunity which is mounted later in the course of the immune response and is naive at the outset, innate immunity provides the first line of defense against microbial agents, while also promoting resolution of inflammation. In the airways, innate immune effector cells mainly consist of eosinophils, neutrophils, mast cells, basophils, macrophages/monocytes, dendritic cells and innate lymphoid cells, which attack pathogens directly or indirectly through the release of inflammatory cytokines and antimicrobial peptides, and coordinate T and B cell-mediated adaptive immunity. Airway epithelial cells are also critically involved in shaping both the innate and adaptive arms of the immune response. Chronic allergic airway inflammation and linked asthmatic disease is often considered a result of aberrant activation of type 2 T helper cells (Th2) towards innocuous environmental allergens; however, innate immune cells are increasingly recognized as key players responsible for the initiation and the perpetuation of allergic responses. Moreover, innate cells participate in immune response regulation through the release of anti-inflammatory mediators, and guide tissue repair and the maintenance of airway homeostasis. The scope of this review is to outline existing knowledge on innate immune responses involved in allergic airway inflammation, highlight current gaps in our understanding of the underlying molecular and cellular mechanisms and discuss the potential use of innate effector cells in new therapeutic avenues. © 2017


Loukeri A.A.,Athens Chest Hospital sotiria | Kampolis C.F.,National and Kapodistrian University of Athens | Ntokou A.,Sotiria General Hospital | Tsoukalas G.,Sotiria General Hospital | Syrigos K.,Sotiria General Hospital
Clinical Lung Cancer | Year: 2015

The average lifelong rate of developing a new primary lung cancer approximates 1% and 6% per year after radical therapy for non-small-cell lung cancer and small cell lung cancer, respectively. The frequency of recorded synchronous and metachronous lung cancers has been increasing in the recent years because of the development of early detection techniques and advances in cancer therapy. The distinction between multiple synchronous or metachronous primary lung cancers and intrapulmonary metastases is based on established clinicopathological criteria, however it is often difficult, although of great importance for the management and prognosis of these patients. Newly developed molecular and genomic methods are expected to contribute to a more solid and clear differentiation. Surgical treatment, whenever feasible, is considered the modality of choice for the management of patients with second primary lung cancers, as opposed to those with metastases. The type and extent of surgery are under discussion. The prognosis of patients with second primary lung cancers largely depends on the time of detection and the stage and location of the second cancer, thus surveillance after surgical resection of the initial tumor is mandatory. © 2015 Elsevier Inc. All rights reserved.


Dimopoulos G.,National and Kapodistrian University of Athens | Lerikou M.,Athens Chest Hospital SOTIRIA | Tsiodras S.,National and Kapodistrian University of Athens | Chranioti A.,National and Kapodistrian University of Athens | And 4 more authors.
Pulmonary Pharmacology and Therapeutics | Year: 2012

The role of viruses in Acute Exacerbations of Chronic Obstructive Pulmonary Disease (AECOPD) needs further elucidation. The aim of the present study was to evaluate the molecular epidemiology of viral pathogens in AECOPD.Patients presenting to the Emergency Room with AECOPD needing hospitalization were recruited. Oropharyngeal and sputum samples were collected in order to perform microarrays-based viral testing for the detection of respiratory viruses.A total of 200 (100%) patients were analyzed and from them in 107 (53.5%) a virus was detected. The commonest identified viruses were the human Respiratory Syncytial Virus (subtypes A and B) (40.5%), influenza virus (subtypes A, B, C) (11%), rhinovirus (8%) and human Parainfluenza Virus (subtypes A and B) (7.5%). A bacterial pathogen was isolated in 27 (14%) patients and a dual infection due to a bacterial and a viral pathogen was recognised in 14/107 patients. Patients with AECOPD and a viral infection had a lengthier hospital stay (9.2±4.6 vs 7.6±4.3, p<0.01) while the severity of the disease was no related with significant differences among the groups of the study population.In conclusion, the isolation of a virus was strongly associated with AECOPD in the examined population. The stage of COPD appeared to have no relation with the frequency of the isolated viruses while dual infection with a viral and a bacterial pathogen was not rare. © 2011 .


Papaioannou A.I.,National and Kapodistrian University of Athens | Kostikas K.,National and Kapodistrian University of Athens | Zervas E.,Athens Chest Hospital Sotiria | Kolilekas L.,Athens Chest Hospital Sotiria | And 2 more authors.
European Respiratory Review | Year: 2015

Although studies show that control of asthma can be achieved in the majority of patients, surveys repeatedly show that this is not the case in real life. Important measures to implement in order to achieve asthma control are trained healthcare professionals, a good patient–doctor relationship, patient education, avoidance of exposure to triggers, personalised management and adherence to treatment. These measures help the majority of asthma patients but have not yet been widely implemented and there should be a concerted action for their implementation. Moreover, further and focused research is needed in severe/refractory asthma. © ERS 2015.


PubMed | Athens Chest Hospital Sotiria, Biomedical Research Foundation of the Academy of Athens and Gothenburg University
Type: Journal Article | Journal: PloS one | Year: 2016

B cells, key cells in allergic inflammation, differentiate in the bone marrow and their precursors include pro-B, pre-B and immature B cells. Eosinophil progenitor cells increase in the lung after allergen exposure. However, the existence and possible role of B cell precursors in the lung during allergic inflammation remains elusive.A BALB/c mouse model of allergic airway inflammation was utilized to perform phenotypic and quantification analyses of pro-B and pre-B cells in the lung by flow cytometry. B cell maturation factors IL-7 and B cell-activating factor (BAFF) and their receptors (CD127 and BAFFR, BCMA, TACI, respectively) were also evaluated in the lung and serum. The effect of anti-BAFF treatment was investigated both in vivo (i.p. administration of BAFF-R-Ig fusion protein) and in vitro (colony forming cell assay). Finally, BAFF levels were examined in the bronchoalveolar lavage (BAL) of asthmatic patients and healthy controls.Precursor pro and pre-B cells increase in the lung after allergen exposure, proliferate in the lung tissue in vivo, express markers of chemotaxis (CCR10 and CXCR4) and co-stimulation (CD40, CD86) and are resistant to apoptosis (Bax). Precursor B cells express receptors for BAFF at baseline, while after allergen challenge both their ligand BAFF and the BCMA receptor expression increases in B cell precursors. Blocking BAFFR in the lung in vivo decreases eosinophils and proliferating precursor B cells. Blocking BAFFR in bone marrow cultures in vitro reduces pre-B colony formation units. BAFF is increased in the BAL of severe asthmatics.Our data support the concept of a BAFF-mediated role for B cell precursors in allergic airway inflammation.


Samitas K.,Asthma Center | Samitas K.,Center for Basic Research | Samitas K.,Gothenburg University | Zervas E.,Asthma Center | And 11 more authors.
European Respiratory Journal | Year: 2011

Recent studies have associated osteopontin (OPN) with allergic inflammation; however, its role in human asthma remains unclear. The aim of this study was to measure OPN levels in the serum, bronchoalveolar lavage fluid (BALF) and bronchial tissue of healthy controls and asthmatics, identify cellular sources of OPN and examine possible correlations between OPN expression, disease severity and airway remodelling. Serum samples were obtained from 35 mild-to-moderate asthmatics, 19 severe asthmatics and 17 healthy controls in the steady state and in cases of exacerbation. Of these subjects, 29 asthmatics and nine controls underwent bronchoscopy with endobronchial biopsy and BALF collection. OPN expression was determined by ELISA and immunohistochemistry/immunofluorescence. Reticular basement membrane thickness and goblet cell hyperplasia were also determined. Serum and BALF OPN levels were significantly increased in all asthmatics in the steady state, whereas serum levels decreased during exacerbations. OPN was upregulated in the bronchial tissue of all patients, and expressed by epithelial, airway and vascular smooth muscle cells, myofibroblasts, T-lymphocytes and mast cells. OPN expression correlated with reticular basement membrane thickness and was more prominent in subepithelial inflammatory cells in severe compared to mild-to-moderate asthma. OPN expression is upregulated in human asthma and associated with remodelling changes, and its subepithelial expression correlates with disease severity. Copyright©ERS 2011.


Bossios A.,Gothenburg University | Sjostrand M.,Gothenburg University | Dahlborn A.-K.,Gothenburg University | Samitas K.,Athens Chest Hospital Sotiria | And 3 more authors.
Allergy: European Journal of Allergy and Clinical Immunology | Year: 2010

Background: Eosinophils develop from hematopoietic CD34+ progenitor cells in the bone marrow (BM) under the influence of Interleukin-5 (IL-5). The primary source of IL-5 is T-lymphocytes, although other sources may exist. The aims of this study were to determine whether CD34+ cells from human peripheral blood (PB) and BM have the capacity to produce IL-5 when stimulated in vitro, and secondly, whether an elevated number of IL-5-producing CD34+ cells can be found in situ in ongoing eosinophilic disease. Methods: CD34+ cells from PB and BM were stimulated in vitro, and IL-5 production and release was assessed by ELISA, ELISPOT, flow cytometry and immunocytochemistry. Blood and BM from a patient with Churg-Strauss syndrome were analyzed by flow cytometry for CD34+/IL-5+ cells, and immunohistochemical staining of CD34+/IL-5+ cells in bronchial biopsies from an asthmatic patient was performed. Results: Both PB and BM CD34+ cells can produce and release IL-5 when stimulated in vitro. In the Churg-Strauss patient, IL-5-producing CD34+ cells were found in PB and BM. Oral glucocorticoid treatment markedly decreased the number of IL-5-positive CD34 cells in the BM. CD34+/IL-5+ cells were present in a patient with asthma. Conclusion: CD34+ cells in blood and BM are capable of producing IL-5 both in vitro and in vivo in humans, arguing that these cells may have the capacity to contribute to eosinophilic inflammation. Consequently, targeting CD34+ progenitor cells that produce and release IL-5 may be effective in reducing the mobilization of eosinophil lineage-committed cells in eosinophilic-driven diseases. © 2009 John Wiley & Sons A/S.


Samitas K.,Athens Chest Hospital Sotiria
Current Opinion in Pulmonary Medicine | Year: 2016

PURPOSE OF REVIEW: Asthma is a heterogeneous disease not only on a clinical but also on a mechanistic level. For a long time, the molecular mechanisms of asthma were considered to be driven by type 2 helper T cells (Th2) and eosinophilic airway inflammation; however, extensive research has revealed that T2-low subtypes that differ from the dominant T2 paradigm are also common. RECENT FINDINGS: Research into asthma pathways has led to the recognition that some asthma phenotypes show absence of T2 inflammation or alternate between T2 and non-T2 responses. Moreover, numerous immune response modifiers that block key-molecules such as interleukin (IL)-5, IL-13, and immunoglobulin E (IgE) have been identified. Along the way, these studies pointed that T2-low inflammation may also be responsible for lack of responsiveness to current treatment regimes. SUMMARY: Asthma pathogenesis is characterized by two major endotypes, a T2-high featuring increased eosinophilic airway inflammation, and a T2-low endotype presenting with either neutrophilic or paucigranulocytic airway inflammation and showing greater resistance to steroids. This clearly presents an unmet therapeutic challenge. A precise definition and characterization of the mechanisms that drive this T2-low inflammatory response in each patient phenotype is necessary to help identify novel drug targets and design more effective and targeted treatments. Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.


Zervas E.,Athens Chest Hospital Sotiria | Samitas K.,Athens Chest Hospital Sotiria | Gaga M.,Athens Chest Hospital Sotiria
International Journal of COPD | Year: 2016

Background: Poor adherence to inhaled therapy is common in patients with asthma and COPD. An inhaler selection based on patients’ preference could be beneficial to adherence and treatment effectiveness. Properly designed questionnaires can assess patients’ satisfaction with their medication devices. The aim of this study was to estimate, using the Feeling of Satisfaction with Inhaler (FSI-10) questionnaire, the ease of use and satisfaction of patients regarding three different marketed dry powder inhalers (DPIs): Diskus®(DK), Elpenhaler®(EH), and Turbuhaler®(TH). The FSI-10 is a self-completed questionnaire to assess patients’ opinions regarding ease of use, portability, and usability of devices, irrespective of the drug used. Patients and methods: We performed a 4-week, open, noninterventional, multicenter, parallel clinical study in 560 asthmatic and 561 COPD patients. During the first visit, patients were classified into three groups according to the DPI they were already using. Patients were regularly receiving their treatments (Seretide DK, Rolenium EH, and Symbicort TH) and agreed to complete the FSI-10 questionnaire in the second visit. Results: A total of 517 COPD and 523 asthma patients completed the study. All DPIs tested received satisfactory results, while the EH obtained consistently higher scores in the FSI-10 in both COPD and asthma patients (44.7 and 44.1 vs 41.5 and 43 for TH, 40.8 and 41.4 for DK, P,0.001 and P,0.01, respectively). TH was rated better than DK by asthma patients. Patients suffering with severe COPD tended to express higher feeling of satisfaction than those with moderate or mild disease, irrespective of the device used. Conclusion: All DPIs tested were highly acceptable by asthma and COPD patients of different ages; nevertheless, EH received significantly higher ratings in most of the questionnaire domains. COPD patients in advanced stages of the disease generally expressed higher level of satisfaction with their devices. © 2016 Zervas et al.

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