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Dive into the research topics where Martina Sterclova is active.

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Featured researches published by Martina Sterclova.


Scandinavian Journal of Immunology | 2009

Bronchoalveolar lavage fluid cellular characteristics, functional parameters and cytokine and chemokine levels in interstitial lung diseases.

Martina Vasakova; Martina Sterclova; L. Kolesar; A. Slavcev; Petr Pohunek; Jan Sulc; J. Skibova; I. Striz

Idiopathic pulmonary fibrosis (IPF), hypersensitivity pneumonitis (HP) and sarcoidosis belong to interstitial lung diseases (ILD) where an imbalance of regulatory, profibrotic and antifibrotic cytokines is hypothesized. The relationship of bronchoalveolar lavage (BAL) fluid (BALF) cytokines, BALF cell profile and ILD course is supposed. The aim of our study was to correlate BALF cytokine and chemokine levels with BALF cellular characteristics and lung function parameters in different ILD. Twenty‐two sarcoidosis, seven IPF and 11 HP patients underwent lung function tests and BAL. The BALF differential cell counts and superficial cell markers were characterized, and MCP‐1, MIP‐1α, MIP‐1β, RANTES, epithelial neutrophil‐activating protein (ENA)‐78, FGF, G‐CSF, GM‐CSF, IFN‐γ, interleukin (IL)‐1α, IL‐1RA, IL‐1β, ‐2β, ‐4β, ‐5β, ‐6β, ‐8β, ‐10β, ‐17β, tumour necrosis factor (TNF)‐α, thromobopoietin (Tpo) and vascular endothelial growth factor (VEGF) values measured. The BALF VEGF values were highest in sarcoidosis (P = 0.0526). IL‐1RA values were higher in IPF and HP compared with sarcoidosis (P = 0.0334). IL‐8/ENA‐78 ratio positively correlated with BALF neutrophil counts in IPF (r = 0.89, P = 0.04). Vital capacity and TLCO values positively correlated with VEGF and negatively with IL‐8 BALF levels in all ILDs but the correlations were most significant in sarcoidosis group. We suppose that VEGF plays a role in ILDs’ early phases and has rather angiogenic than profibrotic effect. On the contrary, IL‐8 is probably upregulated in advanced ILDs with prominent fibrosis and marked lung functions decline. We state that BALF VEGF, IL‐8 and ENA‐78 levels and IL‐8/ENA‐78 ratio could become useful markers of ILDs’ phase, activity and prognosis. They might also be helpful in treatment modality choice.


American Journal of Respiratory and Critical Care Medicine | 2015

Identification of Immune-Relevant Factors Conferring Sarcoidosis Genetic Risk

Annegret Fischer; David Ellinghaus; Marcel Nutsua; Sylvia Hofmann; Courtney G. Montgomery; Michael C. Iannuzzi; Benjamin A. Rybicki; Martin Petrek; Frantisek Mrazek; Stefan Pabst; Christian Grohé; Johan Grunewald; Marcus Ronninger; Anders Eklund; Leonid Padyukov; Violeta Mihailovic-Vucinic; Dragana Jovanovic; Martina Sterclova; Jiri Homolka; Markus M. Nöthen; Stefan Herms; Christian Gieger; Konstantin Strauch; Juliane Winkelmann; Bernhard O. Boehm; Stephan Brand; Carsten Büning; Manfred Schürmann; Eva Ellinghaus; Hansjörg Baurecht

RATIONALE Genetic variation plays a significant role in the etiology of sarcoidosis. However, only a small fraction of its heritability has been explained so far. OBJECTIVES To define further genetic risk loci for sarcoidosis, we used the Immunochip for a candidate gene association study of immune-associated loci. METHODS Altogether the study population comprised over 19,000 individuals. In a two-stage design, 1,726 German sarcoidosis cases and 5,482 control subjects were genotyped for 128,705 single-nucleotide polymorphisms using the Illumina Immunochip for the screening step. The remaining 3,955 cases, 7,514 control subjects, and 684 parents of affected offspring were used for validation and replication of 44 candidate and two established risk single-nucleotide polymorphisms. MEASUREMENTS AND MAIN RESULTS Four novel susceptibility loci were identified with genome-wide significance in the European case-control populations, located on chromosomes 12q24.12 (rs653178; ATXN2/SH2B3), 5q33.3 (rs4921492; IL12B), 4q24 (rs223498; MANBA/NFKB1), and 2q33.2 (rs6748088; FAM117B). We further defined three independent association signals in the HLA region with genome-wide significance, peaking in the BTNL2 promoter region (rs5007259), at HLA-B (rs4143332/HLA-B*0801) and at HLA-DPB1 (rs9277542), and found another novel independent signal near IL23R (rs12069782) on chromosome 1p31.3. CONCLUSIONS Functional predictions and protein network analyses suggest a prominent role of the drug-targetable IL23/Th17 signaling pathway in the genetic etiology of sarcoidosis. Our findings reveal a substantial genetic overlap of sarcoidosis with diverse immune-mediated inflammatory disorders, which could be of relevance for the clinical application of modern therapeutics.


The Lancet Respiratory Medicine | 2017

Antacid therapy in idiopathic pulmonary fibrosis: more questions than answers?

Kerri A. Johannson; Irina Strâmbu; Claudia Ravaglia; Jan C. Grutters; Claudia Valenzuela; Nesrin Mogulkoc; Fabrizio Luppi; Luca Richeldi; Athol U. Wells; Carlo Vancheri; Michael Kreuter; Carlo Albera; Katerina M. Antoniou; Goksel Altinisik; Elisabeth Bendstrup; Benjamin Bondue; Raphael Borie; Kevin K. Brown; Philippe Camus; Diego Castillo; Harold R. Collard; Vincent Cottin; Nunzio Crimi; Giovanni Ferrara; Aryeh Fischer; Jack Gauldie; Thomas Geiser; Andreas Guenther; Nathan Hambly; David M. Hansell

Idiopathic pulmonary fibrosis (IPF) is a progressive parenchymal lung disease of complex cause. Gastro-oesophageal reflux (GER) and microaspiration have been proposed as risk factors for the development and progression of IPF, but robust definitive data are few. A recent international guideline conditionally recommended the use of antacid therapy (proton pump inhibitors or histamine-2-receptor antagonists) for patients with IPF, in the absence of oesophageal reflux or symptoms. In this Position Paper, we summarise the literature addressing the association between GER and IPF, and also identify future research priorities that could clarify this issue. We shed light on the process through which the guideline recommendation was achieved and aim to contextualise the recommendation for providers caring for patients with IPF.


Human Immunology | 2013

IL-4 polymorphisms, HRCT score and lung tissue markers in idiopathic pulmonary fibrosis.

Martina Vasakova; Martina Sterclova; Radoslav Matej; Tomas Olejar; Libor Kolesar; Jelena Skibova; Ilja Striz

AIMS We studied the influence of IL-4 gene polymorphisms on the IPF phenotype, i.e., extent of radiological changes (HRCT interstitial (IS) and alveolar (AS) score) and histopathological markers from lung biopsies. PATIENTS AND METHODS 46 IPF patients underwent genotyping, 43 of them had HRCT and 14 patients had a surgical lung biopsy. The HRCT scans were evaluated for AS and IS. The histopathological evaluation comprised myofibroblast foci (MF), intensity of inflammation and fibrosis (Ashcroft score) and numbers of eosinophils and granulomas. For immunohistochemical evaluation primary antibodies against PAR-2, CD124, TGF beta, YY-1 and TSLP were used. The IL-4 and IL-4 R alpha gene polymorphisms were characterized. RESULTS We found a correlation between eosinophils in lung biopsies and AS. The Ashcroft score was higher in IL-4 HA 2 GCC and MF were more frequent in IL-4 HA 2 TCC carriers. A relationship was found between IL-4 (-1098) A2 T and PAR-2 expression and IL-4 (-590) A1 T, IL-4 HA1TTT and CD124 expression. AS was lower in IL-4 (-590) A1 C, in IL-4 HA1 TCC and in IL-4RA (+1902) A1 A carriers. CONCLUSIONS We suggest that the polymorphisms of IL-4 genes might influence the phenotype of IPF reflected by histopathological changes in lung biopsies and HRCT score.


Clinical Respiratory Journal | 2015

Influence of age on manifestation, VC and TLCO values, and bronchoalveolar lavage cell counts of sarcoidosis and extrinsic allergic alveolitis

Martina Sterclova; Peter Paluch; Jelena Skibova; Martina Vasakova

Immune response probably changes during human life, being influenced by cumulative exposure to environmental factors and individual genetic background.


Scientific Reports | 2016

Glutathione peroxidase 3 localizes to the epithelial lining fluid and the extracellular matrix in interstitial lung disease

Andrea C. Schamberger; Herbert B. Schiller; Isis E. Fernandez; Martina Sterclova; Katharina Heinzelmann; Elisabeth Hennen; Rudolf Hatz; Jürgen Behr; Martina Vasakova; Matthias Mann; Oliver Eickelberg; Claudia A. Staab-Weijnitz

Aberrant antioxidant activity and excessive deposition of extracellular matrix (ECM) are hallmarks of interstitial lung diseases (ILD). It is known that oxidative stress alters the ECM, but extracellular antioxidant defence mechanisms in ILD are incompletely understood. Here, we extracted abundance and detergent solubility of extracellular antioxidant enzymes from a proteomic dataset of bleomycin-induced lung fibrosis in mice and assessed regulation and distribution of glutathione peroxidase 3 (GPX3) in murine and human lung fibrosis. Superoxide dismutase 3 (Sod3), Gpx3, and Gpx activity were increased in mouse BALF during bleomycin-induced lung fibrosis. In lung tissue homogenates, Gpx3, but not Sod3, was upregulated and detergent solubility profiling indicated that Gpx3 associated with ECM proteins. Immunofluorescence analysis showed that Gpx3 was expressed by bronchial epithelial cells and interstitial fibroblasts and localized to the basement membrane and interstitial ECM in lung tissue. As to human ILD samples, BALF of some patients contained high levels of GPX3, and GPX3 was upregulated in lung homogenates from IPF patients. GPX3 expression in primary human bronchial epithelial cells and lung fibroblasts was downregulated by TNF-α, but more variably regulated by TGF-β1 and menadione. In conclusion, the antioxidant enzyme GPX3 localizes to lung ECM and is variably upregulated in ILD.


Experimental and Therapeutic Medicine | 2014

PAR-2, IL-4R, TGF-β and TNF-α in bronchoalveolar lavage distinguishes extrinsic allergic alveolitis from sarcoidosis.

Radoslav Matěj; Magdalena Smětáková; Martina Vasakova; Jana Nováková; Martina Sterclova; Jaromir Kukal; Tomas Olejar

Sarcoidosis (SARC) and extrinsic allergic alveolitis (EAA) share certain markers, making a differential diagnosis difficult even with histopathological investigation. In lung tissue, proteinase-activated receptor-2 (PAR-2) is primarily investigated with regard to epithelial and inflammatory perspectives. Varying levels of certain chemokines can be a useful tool for distinguishing EAA and SARC. Thus, in the present study, differences in the levels of transforming growth factor (TGF)-β1, tumor necrosis factor (TNF)-α, interleukin-4 receptor (IL-4R) and PAR-2 in bronchoalveolar lavage fluid (BALF) were compared, using an ELISA method, between 14 patients with EAA and six patients with SARC. Statistically significant higher levels of IL-4R, PAR-2 and the PAR-2/TGF-β1 and PAR-2/TNF-α ratios were observed in EAA patients as compared with SARC patients. Furthermore, the ratios of TNF-α/total protein, TGF-β1/PAR-2 and TNF-α/PAR-2 were significantly lower in EAA patients than in SARC patients. The results indicated a higher detection of PAR-2 in EAA samples in association with TNF-α and TGF-β levels. As EAA and PAR-2 in parallel belong to the Th2-mediated pathway, the results significantly indicated an association between this receptor and etiology. In addition, the results indicated that SARC is predominantly a granulomatous inflammatory disease, thus, higher levels of TNF-α are observed. Therefore, the detection of PAR-2 and investigated chemokines in BALF may serve as a useful tool in the differential diagnosis between EAA and SARC.


Applied Immunohistochemistry & Molecular Morphology | 2014

Higher TGF-β with lower CD124 and TSLP, but no difference in PAR-2 expression in bronchial biopsy of bronchial asthma patients in comparison with COPD patients.

Radoslav Matěj; Martina Vasakova; Jaromir Kukal; Martina Sterclova; Tomas Olejar

Chronic obstructive pulmonary disease (COPD) and bronchial asthma (BA) are 2 severe respiratory disorders with different predominated immunopathologies. There are several “novel molecules” from different families that are proposed as part of the etiopathogenesis of COPD and BA. Proteinase-activated receptor 2 (PAR-2), thymic stromal lymphoprotein (TSLP), interleukin-4 and its receptor (CD124), Yin-Yang 1 (YY1), and transforming growth factor beta (TGF-&bgr;) have been previously shown to be involved in the pathophysiology of both these diseases. We investigated PAR-2, TSLP, CD124 (interleukin-4R), TGF-&bgr;, and YY1 immunohistochemical expression in endobronchial and transbronchial biopsies from 22 BA patients and 20 COPD patients. Immunostaining for the above-mentioned antigens was quantified using a modified semiquantitative scoring system and statistically evaluated. The values of TGF-&bgr; in the epithelial cells (P=0.0007) and TGF-&bgr; in the submucosa (P=0.0075) were higher in the BA samples, whereas values of CD124 (P=0.0015) and TSLP (P=0.0106) were higher in the COPD samples. No statistically significant differences between the groups were recorded for PAR-2 and YY1. Airway inflammatory reaction diversity in BA and COPD seems to be disease specific; however, there are also shared mechanisms involved in the pathophysiology of both diseases.


Experimental Lung Research | 2009

Chemokine receptors in a regulation of interstitial lung fibrosis and inflammation.

Martina Sterclova; Martina Vasakova; Jan Pavlicek; Monika Metlicka; Eliska Krasna; Ilja Striz

Sarcoidosis and extrinsic allergic alveolitis (EAA) are granulomatous lung diseases with predominantly Th1 immune response. In this prospective study, the authors analyzed the expression of chemokine receptors CXCR2, CXCR3, and CCR3 on bronchoalveolar lavage fluid (BALF) CD4 T cells of patients either with EAA or sarcoidosis. The authors investigated the correlation of chemokine receptors expression, lymphocyte and neutrophil counts in BALF, and high-resolution tomography (HRCT) pattern. Thirteen sarcoidosis and 6 EAA patients were enrolled in the study. The expression of chemokine receptors on BALF CD4 T cells were analyzed by flow cytometry. HRCT scoring system according to Kazerooni was used for evaluation of the disease extent. The authors have found positive correlation between BALF CD4 T-cell CXCR3 expression and HRCT alveolar score in EAA patients (P <. 01). CXCR2 expression on BALF CD4 T cells and interstitial HRCT score did not show a correlation either in the EAA or the sarcoidosis group. Positive correlation between CCR3 expression on CD4+ T cells and HRCT interstitial score was proven in the EAA group (P <. 05). The authors conclude that Th2 predominant immune response may play an important role in chronic EAA pathogenesis. The role of chemokine receptors in the pathogenesis of EAA and sarcoidosis should be presumed and investigated.


European Respiratory Journal | 2018

Phenotypes of organ involvement in sarcoidosis

Jonas Schupp; Sandra Freitag-Wolf; Elena Bargagli; Violeta Mihailović-Vučinić; Paola Rottoli; Aleksandar Grubanovic; Arne Jochens; Lukas Tittmann; Jasmin Schnerch; Carmela Olivieri; Annegret Fischer; Dragana Jovanovic; Snežana Filipovic; Jelica Videnovic-Ivanovic; Paul Bresser; René E. Jonkers; Kate O'Reilly; Ling-Pei Ho; Karoline I. Gaede; Peter Zabel; Anna Dubaniewicz; Ben Marshall; Robert Kieszko; Janusz Milanowski; Andreas Günther; Anette Weihrich; Martin Petrek; Vitezslav Kolek; Michael P. Keane; Sarah L. O'Beirne

Sarcoidosis is a highly variable, systemic granulomatous disease of hitherto unknown aetiology. The GenPhenReSa (Genotype–Phenotype Relationship in Sarcoidosis) project represents a European multicentre study to investigate the influence of genotype on disease phenotypes in sarcoidosis. The baseline phenotype module of GenPhenReSa comprised 2163 Caucasian patients with sarcoidosis who were phenotyped at 31 study centres according to a standardised protocol. From this module, we found that patients with acute onset were mainly female, young and of Scadding type I or II. Female patients showed a significantly higher frequency of eye and skin involvement, and complained more of fatigue. Based on multidimensional correspondence analysis and subsequent cluster analysis, patients could be clearly stratified into five distinct, yet undescribed, subgroups according to predominant organ involvement: 1) abdominal organ involvement, 2) ocular–cardiac–cutaneous–central nervous system disease involvement, 3) musculoskeletal–cutaneous involvement, 4) pulmonary and intrathoracic lymph node involvement, and 5) extrapulmonary involvement. These five new clinical phenotypes will be useful to recruit homogenous cohorts in future biomedical studies. Five new clinical phenotypes of sarcoidosis have been identified by analysing organ manifestations of 1932 patients http://ow.ly/UYLC30jpUkq

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Martina Vasakova

Charles University in Prague

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Peter Paluch

Charles University in Prague

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Vladimír Bartoš

Charles University in Prague

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Martina Plačková

Charles University in Prague

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Pavlína Lisá

Charles University in Prague

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Radka Bittenglová

Charles University in Prague

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Petra Mandakova

Charles University in Prague

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