Magdalena Paplińska‐Goryca

Medical University of Warsaw

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Rafał Krenke

Medical University of Warsaw

Patrycja Nejman‐Gryz

Medical University of Warsaw

Katarzyna Górska

Medical University of Warsaw

Małgorzata Proboszcz

Medical University of Warsaw

Paulina Misiukiewicz‐Stępień

Medical University of Warsaw

Ryszarda Chazan

Medical University of Warsaw

Marta Maskey‐Warzęchowska

Medical University of Warsaw

Renata Rubinsztajn

Medical University of Warsaw

Joanna Hermanowicz-Salamon

Medical University of Warsaw

Tadeusz Przybyłowski

Medical University of Warsaw

Cooperative Institutions

Medical University of Warsaw

Centralny Szpital Kliniczny

OncoArendi Therapeutics (Poland)

University of Warsaw

Wojskowy Instytut Medyczny

Johns Hopkins University

Central Clinical Hospital

Johns Hopkins Medicine

Johns Hopkins Hospital

Polish Academy of Sciences

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Periostin concentration in exhaled breath condensate in children with mild asthma

Journal of Asthma (2019)

Patrycja Nejman‐Gryz Katarzyna Górska Katarzyna Krenke Joanna Peradzyńska Magdalena Paplińska‐Goryca

Periostin is considered to be a marker of eosinophilic inflammation in patients with asthma. However, there are no literature data on exhaled breath condensate (EBC) periostin level in pediatric patients with asthma. The aim of this study was to analyze EBC periostin concentration in children with mild asthma and to evaluate the potential usefulness of EBC periostin level as a biomarker for the disease.EBC and serum periostin concentrations were measured by enzyme-linked immunosorbent assay in 23 children with asthma and 23 healthy controls.EBC periostin concentration was 250- to 780-fold lower than that found in serum. No significant differences between serum nor EBC periostin concentration in asthmatics and the control group were showed. The comparison between children with Th2 and non-Th2 type of asthma did not show significant differences in periostin concentration, both in serum and EBC. Serum periostin concentration inversely correlated with BMI and age not only in asthma patients but also in controls.In children with mild asthma, periostin may be measured not only in serum but also in EBC. The low periostin level in patients with mild asthma and lack of difference between asthmatic subjects and controls indicate that EBC periostin may not be useful as an asthma biomarker in this group.

Periostin

Exhaled breath condensate

10.1080/02770903.2019.1659312

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Citations (10)

Clinical Development of OATD-01 - a Novel, Chitinase Inhibitor for Treatment of Interstitial Lung Diseases

R. Dyjas Joanna Lipner Barbara Dymek Michał Mlącki Agnieszka Zagożdżon

Chitinase

10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5623

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The expression of IL17RA on sputum macrophages in asthma patients

Cytokine (2021)

Patrycja Nejman‐Gryz Magdalena Paplińska‐Goryca Małgorzata Proboszcz Magdalena Grabczak Joanna Hermanowicz-Salamon

IL-17A and IL-25 (IL-17 cytokines family) play an important role in the development of asthma, and allergy. Both cytokines act by binding to heterodimeric receptors with IL17RA as a common subunit. This receptor is found on macrophages, and some other cell types. The aim of the study was to determine the expression of IL17RA on asthmatic and control macrophages from induced sputum (IS) with the regard to IL-17/IL-25 background and relation to clinical features of the disease. We found an elevated expression of IL17RA on sputum macrophages in asthma patients vs controls. A characteristic sputum profile of atopic asthmatic was as follows: high CD206 + IL17RA + macrophage percentage, elevated IL-25 level and low CD206 + IL17RA- macrophage percentage. Based on the above results, it seems that CD206 + sputum macrophages are the effector cells that express common subunit of the receptor for IL-17A and IL-25 in asthma. This may be related to the Th2-dependent environment in asthma and increased concentrations of IL-25 and IL-13 as well as eosinophils in the airways. To our knowledge, our study provides the first data on a possible link between immunological reaction orchestrating CD206 + expressing sputum macrophages and IL-25 via IL17RA pathway in the asthmatic airways.

10.1016/j.cyto.2021.155518

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Primary human mesothelial cell culture in the evaluation of the inflammatory response to different sclerosing agents used for pleurodesis

Physiological Reports (2021)

Michał Mierzejewski Magdalena Paplińska‐Goryca Piotr Korczyński Rafał Krenke

The mechanisms of chemical pleurodesis are still not fully explained. We aimed to evaluate the feasibility of using primary biopsy-derived human mesothelial cells to establish an in vitro culture and to assess the response of pleural mesothelial cells to different sclerosing agents. Talc, povidone-iodine, doxycycline, and TGF-β were used at different doses to stimulate pleural mesothelial cells. After 6 and 24 h, mRNA expression of interleukin (IL)-1β, IL-6, IL-8, TGF-β, MCP-1, IL-17A, and MMP9 was measured in cultured cells, and the protein level of IL-1β, IL-6, and IL-8 was measured in the culture supernatant. The most pronounced response was observed after talc exposure. It was expressed as an increase in IL-1β concentration in culture supernatant after 24 h of higher talc dose stimulation compared to 6 h of stimulation (17.14 pg/ml [11.96-33.32 pg/ml] vs. 1.84 pg/ml [1.81-1.90 pg/ml], p = 0.02). We showed that culture pleural mesothelial cells isolated from pleura biopsy specimens is feasible. Inflammatory responses of mesothelial cells to different sclerosants were highly variable with no consistent pattern of mesothelium reaction neither in terms of different sclerosing agents nor in the time of the most significant reaction. We demonstrated that pro-inflammatory mesothelial response includes an increase in IL-1β mRNA expression and protein production. This may suggest the role of IL-1β in the formation and maintenance of the inflammatory response during pleurodesis.

Mesothelium

Pleurodesis

Interleukin 8

10.14814/phy2.14846

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Citations (7)

Pleural fluid adenosine deaminase and interferon gamma as diagnostic tools in tuberculosis pleurisy.

PubMed (2008)

Rafał Krenke Aleksandra Safianowska Magdalena Paplińska‐Goryca Jacek Nasiłowski Barbara Dmowska-Sobstyl

Several biological markers have been proposed to improve the efficacy of diagnosing tuberculous pleurisy. The study was undertaken to evaluate the accuracy of pleural fluid adenosine deaminase (ADA) activity and interferon-gamma (IFN-gamma) concentration in differentiating tuberculous pleural effusion (TPE) and nontuberculous pleural effusion (non-TPE). Ninety four patients (50 M and 44 F, mean age 60+/-18, range 18-95 years) with pleural effusion (PE) were studied. TPE was diagnosed in patients with: (i) positive pleural fluid or pleural biopsy culture or (ii) granulomas in the pleural biopsy specimen, after exclusion of other granulomatous diseases. Pleural fluid ADA activity was measured with the colorimetric method of Giusti, while IFN-gamma level was measured with ELISA. TPE was diagnosed in 28 patients. The non-TPE group consisted of 35 patients with malignant PE, 20 patients with parapneumonic effusion/pleural empyema, 5 with pleural transudate, and 6 with miscellaneous PE. The ADA activity and IFN-gamma concentration were significantly higher in TPE than in non-TPE (614.1+/-324.5 vs. 15.1+/-36.0 pg/ml, P<0.0001 and 75.1+/-39.1 vs. 11.0+/-16.6 U/l respectively, P<0.0001). The diagnostic sensitivity and specificity of IFN-gamma measurement (cut-off value of 75.0 pg/ml) were 100% and 98.5% respectively and were similar to those of ADA (100% and 93.9% at the cut-off value of 40.3 U/L). We conclude that pleural fluid ADA activity and IFN-gamma concentration are highly sensitive and specific markers of tuberculous pleurisy.

Parapneumonic effusion

Pleurisy

Thoracoscopy

Pleural disease

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Citations (40)

Sputum cytokine profiling according to the type of airway inflammation in obstructive pulmonary diseases

03.02 - Airway cell biology and immunopathology (2018)

Małgorzata Proboszcz Patrycja Nejman‐Gryz Magdalena Paplińska‐Goryca Katarzyna Górska Rafał Krenke

Aims and objectives: Airway inflammation in asthma and COPD displays overlapping features. The aim of the study was to test the hypothesis that the profile of cytokines in induced sputum (IS) from asthma and COPD patients is related to the type of inflammation rather than to the underlying disease. Methods: IS was collected from corticosteroid naïve patients with mild-to-moderate asthma (n=30) and COPD (n=30). Total and differential cell counts in IS were assessed and the concentration of 35 cytokines were measured in IS supernatant by Luminex platform or ELISA assay. Results: Concentrations of a number of cytokines, including IL-6, IL-8, GM-CSF, IFNγ and VEGF were significantly different (p<0.05) in asthma and COPD patients. However, even the more pronounced differences were found when patients with neutrophilic vs. non-neutrophilic airway inflammation (regardless of the underlying disease) were compared. This referred to eotaxin-2, neutrophil elastase, TSLP, IL-6, IL-7, IL-8, IL-12, G-CSF, IP-10, MCP-1, MIP-1a, MIP-1b, TNFα (p<0.05). Surprisingly, eotaxin-1 was the only cytokine differentiating eosinophilic vs. non-eosinophilic airway inflammation. Conclusions: Our study demonstrated that a broad spectrum of cytokines is involved in airway inflammation in obstructive airway diseases and that defining a type of airway inflammation based on IS analysis might be an alternative approach in patients with obstructive airway disease usually classified as asthma or COPD. This seems to be consistent with the concept of "treatable traits" and personalized approach to treatment.

Profiling (computer programming)

10.1183/13993003.congress-2018.pa963

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Genetic characterization of macrophages from induced sputum of asthma and COPD patients

Magdalena Paplińska‐Goryca

Characterization

10.26226/morressier.5acdc65ed462b8029238d8fe

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The effect of 1,25-dihydroxyvitamin D3 on TSLP, IL-33 and IL-25 expression in respiratory epithelium

European Cytokine Network (2016)

Magdalena Paplińska‐Goryca Patrycja Nejman‐Gryz Małgorzata Proboszcz Rafał Krenke

Airway epithelium is an active and important component of the immunological response in the pathophysiology of obstructive lung diseases. Recent studies suggest an important role for vitamin D3 in asthma severity and treatment response. Our study evaluated the influence of an active form of vitamin D3 on the expression of selected mediators of allergic inflammation in the respiratory epithelium. Primary nasal and bronchial epithelial cells were exposed to1,25D3 for 1 hour and were then stimulated or not with IL-4, TNF-α, LPS, and poly I:C. After 24 hours TSLP, IL-33, and IL-25 protein levels were measured in culture supernatants using ELISA and mRNA levels in cells by real time PCR. 1,25D3 increased TSLP concentration in unstimulated nasal epithelial cells, but did not influence IL-33 and IL-25 expression. In IL-4-stimulated epithelial cell cultures 1,25D3 mostly inhibited TSLP and IL-33 expression. In LPS-treated cultures 1,25D3 decreased IL-33 expression. Simultaneously 1,25D3 augmented IL-25 production in the same model of stimulation. Our study revealed the dual nature of vitamin D3 manifested in both pro- and anti-inflammatory properties observed in airway epithelial cells.

Respiratory tract

10.1684/ecn.2016.0377

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Epithelial derived cytokines IL-25, IL-33 and TSLP in obstructive lung diseases

Patrycja Nejman‐Gryz Katarzyna Górska Magdalena Paplińska‐Goryca Małgorzata Proboszcz Rafał Krenke

An epithelium-derived cytokines represent a master switch at the interface between environmental allergens and pulmonary immunologic response. IL-33, IL-25, and TSLP are released by airway epithelial cells and may affect innate lymphoid cells (ILC2). These cells are a rich source of Th2 cytokines, that are involved in airway eosinophilia, mucus production and airway hyperreactivit. The aim of the study was to define the TSLP, IL-25 and IL-33 expression and its correlation with clinical features of obstructive lung diseases. Methods: the study enrolled 38 patients: 12 of IgE-mediated asthma, 16 with COPD and 10 controls who underwent lung function test and sputum induction. In induced sputum (IS) mRNA and protein expression levels of TSLP, IL-25 and IL-33 were evaluated (using real-time PCR and ELISA method, respectively). Results: both asthma and COPD patients had elevated concentration of TSLP, IL-25 and IL-33 in IS vs. control. Significantly higher eosinophil percentage in IS was found in asthmatics compared to controls, while COPD group were characterized by increased percentage of IS neutrophils vs controls. There were no significant differences between IS levels of TSLP, IL-25 and IL-33 and their mRNA expression in asthma vs COPD patients. In all groups IS concentration of TSLP and IL-25 correlated positively with the percentage of neutrophils in IS and with the value of FEV1% and FEV1%VC. Conclusions: TSLP, IL-25 and IL-33 expression is elevated in obstructive lung diseases. Th2 mediated immunological response could be observed not only in asthma but also in COPD. The result of this study warrant further evaluation of the role of these cytokines in particular phenotypes of asthma and COPD.

Proinflammatory cytokine

10.1183/1393003.congress-2017.pa571

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Citations (1)

Rola eotaksyn w patofizjologii astmy

Advances in respiratory medicine (2007)

Magdalena Paplińska‐Goryca H Grubek-Jaworska Ryszarda Chazan

Astma wiąże się z napływem eozynofilów do dróg oddechowych. Eozynofile odgrywają ważną rolę w patogenezie tej choroby. Interleukina-5 jest głównym czynnikiem regulującym proliferację, dojrzewanie i dystrybucję eozynofilów, mimo że ostatnie badania sugerują, że poza IL-5 w patogenezie astmy może uczestniczyć eotaksyna. Eotaksyna jest CC chemokiną po raz pierwszy odkrytą w płynie z płukania oskrzelikowo-pęcherzykowego u świnki morskiej. Eotaksyna łączy się selektywnie z receptorem CCR3 obecnym na eozynofilach, bazofilach i mastocytach, co może wiązać się z patogenezą astmy. Jest ona wytwarzana przez komórki nabłonka płuc i jelit, pośredniczy w preferencyjnej rekrutacji eozynofilów do tych organów. Produkcję eotaksyny stymuluje IL-4, IL-13, TNF-α. Obecnie znane są trzy eotaksyny ludzkie: eotaksyna-1 (CCL11), eotaksyna- 2 (CCL24) i eotaksyna-3 (CCL26). Przypuszcza się, że ekspresja eotaksyny-3 może być następstwem prowokacji alergenowej. W badaniach na hodowlach komórkowych in vitro wykazano pewne działanie hamujące glikokortykosteroidów na produkcję eotaksyn. Danych klinicznych dotyczących wpływu leczenia kortykosteroidami na stężenie eotaksyn nie ma zbyt wiele. Receptor CCR3 bierze się pod uwagę jako cel terapeutyczny w astmie oskrzelowej.

10.5603/arm.27997

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Citations (11)