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21 results on '"Olszewska-Ziąber, A"'

2. Inflammatory endotypes of chronic rhinosinusitis based on cluster analysis of biomarkers

Author

Tomassen, Peter, Vandeplas, Griet, Van Zele, Thibaut, Cardell, Lars-Olaf, Arebro, Julia, Olze, Heidi, Förster-Ruhrmann, Ulrike, Kowalski, Marek L., Olszewska-Ziąber, Agnieszka, Holtappels, Gabriele, De Ruyck, Natalie, Wang, Xiangdong, Van Drunen, Cornelis, Mullol, Joaquim, Hellings, Peter, Hox, Valerie, Toskala, Elina, Scadding, Glenis, Lund, Valerie, Zhang, Luo, Fokkens, Wytske, and Bachert, Claus

Published
2016
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4. Enhanced inhibition of nasal epithelial cell repair by innate stimulation in patients with allergic rhinitis

Author

Anna, Lewandowska-Polak, Brauncajs Małgorzata, Jarzębska Marzanna, Olszewska-Ziąber Agnieszka, Makowska Joanna, and Kowalski Marek, L.

Subjects
wound repair, LPS, TLRs, nasal epithelium, poly (I:C)
Abstract

Introduction. Impaired repair of airway epithelium may lead to persistence of inflammation and remodelling. Regeneration of injured epithelium is a complex phenomenon and the role of toll-like receptors (TLRs) and respiratory virus products in this process have not been established. Aim of the study. In this study we aimed to test if wound repair in nasal epithelial cells is modulated by microbial products and if this process was different in patients with allergic rhinitis and in healthy subjects. Materials and methods. Injured human nasal epithelial cells (hNECs) monolayers were incubated with the toll-like receptors agonists: poly (I:C) and lipopolisacharide (LPS); allergen Der p1, and supernatants from virus-infected epithelial cells. Regeneration of injured epithelium was assessed by measuring changes in the area of epithelial damage. Results. Addition of either poly (I:C) or LPS induced a dose depen-dant inhibition of wound repair in hNECs monolayers. Supernatants from RV1b-infected cells decreased epithelial cell regeneration after mechanical injury only in allergic patients. At baseline conditions the dynamics of epithelial repair was similar in allergic and non-allergic epithelium. However, inhibitory effects of innate stimuli on epithelial repair was stronger in patients with allergic rhinitis as compared to healthy individuals. Conclusions. This study showed that microbial products may affect regeneration of the nasal epithelium, and allergic patients are more susceptible to suppression of epithelial regeneration

Published
2019
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5. Clinical benefits of aspirin desensitization in patients with nonsteroidal anti-inflammatory drug exacerbated respiratory disease are not related to urinary eicosanoid release and are accompanied with decreased urine creatinine

Author

Marcin Kurowski, Anna Lewandowska-Polak, Marek L. Kowalski, Arkadiusz Rotkiewicz, Agnieszka Olszewska-Ziąber, Bartłomiej Woźniakowski, Barbara Bieńkiewicz, and Joanna Makowska

Subjects
Adult, Pulmonary and Respiratory Medicine, Leukotrienes, medicine.medical_specialty, Urinary system, medicine.medical_treatment, Respiratory Tract Diseases, Urine, Gastroenterology, Drug Hypersensitivity, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Internal medicine, medicine, Humans, Immunology and Allergy, Sinusitis, 030223 otorhinolaryngology, Asthma, Desensitization (medicine), Creatinine, Aspirin, Prostaglandin D2, business.industry, Anti-Inflammatory Agents, Non-Steroidal, Respiratory disease, General Medicine, Creatine, medicine.disease, 030228 respiratory system, chemistry, Eicosanoid, Desensitization, Immunologic, Anesthesia, Eicosanoids, business, medicine.drug
Abstract

Background Treatment with acetylsalicylic acid (ASA) after desensitization may be a therapeutic option in patients with nonsteroidal anti-inflammatory drug exacerbated respiratory disease (NERD). The mechanisms that lead to improvement in rhinosinusitis and asthma symptoms remain unknown. Aim To attribute the documented clinical effects of ASA treatment of chronic rhinosinusitis and/or asthma to the release of eicosanoid metabolites in urine. Methods Fourteen patients with NERD were successfully desensitized, and, eventually, eight patients were treated with 650 mg of ASA daily for 3 months. In addition to clinical assessments, nuclear magnetic resonance imaging and smell test were performed before and after treatment with ASA. Venous blood and urine were collected before desensitization and after 1 and 3 months of treatment. The levels of urinary leukotrienes (LT) (cysteinyl LT and LTE4) and tetranor PGDM (metabolite of prostaglandin D2) were measured by enzyme-linked immunosorbent assay. Results Treatment with ASA after desensitization alleviated symptoms of rhinosinusitis, improved nasal patency (mean, 50% decrease in peak nasal inspiratory flow) and sense of smell (fourfold increase in smell test score) in as early as 4 weeks. Clinical improvements were not accompanied by any change in sinonasal mucosa thickness as assessed with nuclear magnetic resonance. Urinary cysteinyl LTs, LTE4, and prostaglandin D2 metabolite remained relatively stable during ASA treatment and did not correlate with clinical improvements. Desensitization was associated with a progressive decrease of urinary creatinine. Conclusion Clinical improvement in rhinosinusitis and/or asthma after ASA desensitization was not related to concentrations of urinary eicosanoid metabolites. A decrease of urinary creatinine requires further study to determine the renal safety of long-term treatment with ASA after desensitization.

Published
2016
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6. Impaired virus replication and decreased innate immune responses to viral infections in nasal epithelial cells from patients with allergic rhinitis

Author

Głobińska, A. Pawełczyk, M. Piechota-Polańczyk, A. Olszewska-Ziąber, A. Moskwa, S. Mikołajczyk, A. Jabłońska, A. Zakrzewski, P.K. Brauncajs, M. Jarzębska, M. Taka, S. Papadopoulos, N.G. Kowalski, M.L.

Abstract

The aim of this study was to assess the immune response to parainfluenza virus type 3 (PIV3), rhinovirus 1B (RV1B) and intracellular Toll-like receptors (TLR) agonists in nasal epithelial cells (NECs) from patients with allergic rhinitis and healthy controls. NECs were obtained from eight patients with allergic rhinitis (AR) and 11 non-atopic healthy controls (HC) by nasal scraping, grown to confluence and exposed to PIV3, RV1B infection or TLR-3 and TLR-7/8 agonists. Interferon (IFN)-λ1, IFN-α, IFN-β and regulated on activation, normal T expressed and secreted (RANTES) release into the cell culture supernatants was assessed at 8, 24 and 48 h upon infection or 8 and 24 h after stimulation with poly(I:C) and R848. mRNA levels of IFNs, RANTES, interferon regulatory transcription factor (IRF)3, IRF7 and viral gene copy number were determined using real-time polymerase chain reaction (RT-PCR). PIV3 but not RV1B replication 48 h after infection was significantly lower (P < 0·01) in NECs from AR patients compared to HC. PIV3 infection induced significantly less IFN-λ1 (both protein and mRNA) in NECs from AR compared to HC. IFN-β mRNA expression and RANTES protein release and mRNA expression tended to be smaller in AR compared HC cells in response to both viruses. Stimulation with TLR-3 agonist [poly (I:C)] induced similar IFN-λ1 and RANTES generation in AR and HC subjects. Viral infections in NECs induced IRF7 expression, which correlated with IFN and RANTES expression. These data suggest that virus proliferation rates and the immune response profile are different in nasal epithelial cells from patients with allergic rhinitis compared to healthy individuals. © 2016 British Society for Immunology

Published
2017

7. Impaired virus replication and decreased innate immune responses to viral infections in nasal epithelial cells from patients with allergic rhinitis

Author

P K Zakrzewski, Sylwia Moskwa, A. Mikołajczyk, Marek L. Kowalski, Agnieszka Jablonska, Nikolaos G. Papadopoulos, Marzanna Jarzębska, Styliani Taka, Anna Głobińska, Agnieszka Olszewska-Ziąber, M Brauncajs, Małgorzata Pawełczyk, and Aleksandra Piechota-Polanczyk

Subjects
0301 basic medicine, Adult, Male, Rhinovirus, Interferon Regulatory Factor-7, Immunology, Common Cold, Nose, medicine.disease_cause, Virus Replication, Respirovirus Infections, Virus, 03 medical and health sciences, Young Adult, 0302 clinical medicine, Immune system, Interferon, Immunology and Allergy, Medicine, Humans, Chemokine CCL5, Cells, Cultured, Innate immune system, business.industry, Imidazoles, Epithelial Cells, Original Articles, Middle Aged, Rhinitis, Allergic, Immunity, Innate, Parainfluenza Virus 3, Human, Toll-Like Receptor 3, 030104 developmental biology, Poly I-C, 030228 respiratory system, Viral replication, Toll-Like Receptor 7, Cell culture, IRF7, Female, Interferons, business, medicine.drug
Abstract

Summary The aim of this study was to assess the immune response to parainfluenza virus type 3 (PIV3), rhinovirus 1B (RV1B) and intracellular Toll-like receptors (TLR) agonists in nasal epithelial cells (NECs) from patients with allergic rhinitis and healthy controls. NECs were obtained from eight patients with allergic rhinitis (AR) and 11 non-atopic healthy controls (HC) by nasal scraping, grown to confluence and exposed to PIV3, RV1B infection or TLR-3 and TLR-7/8 agonists. Interferon (IFN)-λ1, IFN-α, IFN-β and regulated on activation, normal T expressed and secreted (RANTES) release into the cell culture supernatants was assessed at 8, 24 and 48 h upon infection or 8 and 24 h after stimulation with poly(I:C) and R848. mRNA levels of IFNs, RANTES, interferon regulatory transcription factor (IRF)3, IRF7 and viral gene copy number were determined using real-time polymerase chain reaction (RT-PCR). PIV3 but not RV1B replication 48 h after infection was significantly lower (P

Published
2016

8. Serious Asthma Events with Fluticasone plus Salmeterol versus Fluticasone Alone

Author

Stempel, Da, Raphiou, Ih, Kral, Km, Yeakey, Am, Emmett, Ah, Prazma, Cm, Buaron, Ks, Pascoe, Sj, Austri, Investigators, Altieri, Hh, Antuni, Jd, Bergna, Ma, Cuadrado, Ja, De Gennaro MS, Fazio Lizandrelo CL, Gattolin, G, Gosn, Am, Larrateguy, Ld, Marcipar, Am, Maspero, Jf, Medina, Iv, Perez Chada RD, Silva, D, Victorio, Cf, Bardin, Pg, Carroll, Pa, Clements, Bs, Dore, Nd, Robinson, Pd, Fitzgerald, Da, Robinson, Pj, Russo, Ma, Sajkov, D, Thomas, Ps, Upham, Jw, Forstner, B, Kaik, G, Koeberl, Gh, Studnicka, M, Wallner, G, Balthazar, Y, Bauler, A, Dupont, Lj, Martinot, Jb, Ninane, V, Peché, R, Pilette, C, Dimitrova, R, Dimova, D, Kissyova Ibrishimova, G, Loboshka Becheva, M, Machkovska, M, Madjarov, S, Mandazhieva Pepelanova, M, Naidenova, I, Noleva, K, Takovska, N, Terziev, C, Aggarwal, Nk, Chapman, Kr, Csanadi, Ma, Dhillon, R, Henein, S, Kelly, Aj, Lam, As, Liem, Jj, Lougheed, Md, Lowe, Dw, Rizvi, Q, van den Berg, L, Zidel, B, Barros Monge MJ, Calvo Gil MA, Castillo Hofer CR, Diaz Amor PV, Lezana Soya, V, Quilodran Silva CN, Bolivar Grimaldos, F, Solarte-Rodriguez, I, Butkovic-Tomljanovic, R, Hegedus-Jungvirth, M, Ivkovic-Jurekovic, I, Simunov-Karuza, G, Buresova, M, Bursova, J, Fratrik, J, Guttlerova, E, Hartman, P, Jirmanova, I, Kalina, P, Kolman, P, Kucera, M, Povysilova, L, Pravda, P, Svabkova, A, Zakova, L, Backer, V, Maltbaek, N, Johnsen, Cr, Aries, Sp, Babyesiza, A, Barth, D, Benedix, A, Berg, P, Bergtholdt, B, Bettig, U, Bindig, Hw, Botzen, U, Brehler, R, Breyer, Go, Bruckhaus-Walter, M, Dapper, T, Eckhard, Jg, Engelhard, R, Feldmeyer, F, Fissan, H, Franz, Kh, Frick, Bs, Funck, J, Gessner, Cm, Ginko, T, Grigat, Ce, Grimm-Sachs, V, Groth, G, Hampf, J, Hanf, G, Havasi-Jost, G, Heinz, Gu, Helm, K, Hoeltz, S, Hofmann, S, Jander, R, Jandl, M, Jasch-Hoppe, B, Jung, T, Junggeburth, Jj, Kardos, P, Knueppel, W, Koch, T, Kolorz, C, Korduan, M, Korth-Wiemann, B, Krezdorn, Hg, Kroker, A, Kruell, M, Kuehne, P, Lenk, U, Liefring, E, Merke, J, Micke, L, Mitlehner, W, Mueller, H, Naudts, If, Neumann, G, Oldenburg, W, Overlack, A, Panzer, F, Reinholz, N, Remppis, R, Riegel, P, Rueckert, P, Schaetzl, Rj, Schauer, U, Hamelmann, E, Schenkenberger, I, Schlegel, V, Scholz, G, Schroers, M, Schwittay, A, Sebert, M, Tyler, K, Soemantri, Pa, Stock, P, Stuchlik, G, Unland, M, von Mallinckrodt, C, Wachter, J, Weber, U, Weberling, F, Wehgartner-Winkler, S, Weimer, J, Wiemer, S, Winkelmann, Ej, Zeisler, Kh, Ziegner, A, Zimny, Hh, Andrasofszky, Z, Bartha, A, Farkas, M, Gömöri, K, Kis, S, Major, K, Mészáros, I, Mezei, M, Rakvacs, M, Szalai, Z, Szántó, J, Szentesi, M, Szolnoki, E, Valyon, E, Zibotics, H, Anwar, J, Arimah, C, Djajalaksana, S, Rai, Ib, Setijadi, Ar, Setyanto, Db, Susanti, F, Syafiuddin, T, Syamsi, Ln, Wijanarko, P, Yunus, F, Bonavia, M, Braga, M, Chetta, Aa, Cerveri, I, Luisetti, M, Crimi, N, Cutrera, R, De Rosa, M, Esposito, S, Foresi, A, Gammeri, E, Iemoli, E, Legnani, Dl, Michetti, G, Pastorello, Ea, Pesci, A, Pistolesi, M, Riva, E, Romano, A, Scichilone, N, Terracciano, L, Tripodi, S, Choi, I, Kim, C, Kim, Js, Kim, Wj, Koh, Yy, Kwon, Ss, Lee, Sh, Lee, S, Lee, Sk, Park, Cs, Cirule, I, Eglite, R, Petrova, I, Poga, M, Smiltena, I, Chomiciene, A, Davoliene, I, Griskeviciene, V, Naudziunas, A, Naudziunas, S, Rudzeviciene, O, Sitkauskiene, B, Urbonas, G, Vaicius, D, Valavicius, A, Valiulis, A, Vebriene, J, bin Abdul Aziz FA, Daud, M, Ismail, Ai, Tengku Saifudin TI, Md Kassim RM, Mohd Fadzli FB, Wan Mohamad WH, Aguilar Dominguez PE, Aguilar-Orozco, Ra, Garza-Salinas, S, Ramirez-Diaz, Sp, Sánchez Llamas, F, Soto-Ramos, M, Velarde-Mora, Hj, Aguirre Sosa, I, Cisneros, Am, Estrella Viladegut RA, Matsuno Fuchigami, A, Adiaz-Baui, Tt, Bernan, Ap, Onia, Af, Sandagon, Mj, S-Naval, S, Yu, Cy, Bartuzi, Z, Bielous-Wilk, A, Błażowski, Ł, Bożek, A, Brzostek, J, Chorostowska-Wynimko, J, Ciekalska, K, Ziora, D, Cieslicki, J, Emeryk, A, Folcik, K, Gałuszka-Bilińska, A, Gawlik, R, Giejlo, M, Harat, R, Hofman, T, Jahnz-Różyk, K, Jedrzejczak, M, Kachel, T, Kamiński, D, Kelm Warchol, A, Konieczny, Z, Kwasniewski, A, Leszczyński, W, Mincewicz, G, Niezgoda, K, Olszewska-Ziąber, A, Onasz-Manitius, M, Pawlukiewicz, M, Piotrowicz, P, Piotrowski, W, Pisarczyk-Bogacka, E, Piskorz, P, Prokop-Staszecka, A, Roslan, A, Słomka, A, Smalera, E, Stelmach, I, Swierczynska-Krepa, M, Szmidt, M, Tarnowska-Matusiak, M, Tłuczykont, B, Tyminska, K, Waszkuc-Golonko, J, Wojciechowska, I, Alexandrescu, Ds, Neamtu, Ml, Todea, D, Alekseeva, E, Aleksandrova, E, Asherova, I, Barbarash, Ol, Bugrova, O, Bukreeva, Eb, Chermenskiy, A, Chizhova, O, Demko, I, Evdokimova, A, Giorgadze, Ml, Grigoryev, S, Irkhina, I, Khurkhurova, Nv, Kondyurina, Eg, Kostin, Vi, Kudelya, L, Laleko, Sl, Lenskaya, L, Levashov, S, Logvinenko, N, Martynov, A, Mizernitski, Y, Nemtsov, B, Novozhenov, Vg, Pavlishchuk, S, Popova, Vv, Reshetko, Ov, Sherenkov, A, Shirinsky, Vs, Shpagina, L, Soloviev, Ki, Tkachev, A, Trofimov, Vi, Vertkin, Al, Vorobeva, E, Idrisova, E, Yakushin, S, Zadionchenko, V, Zhiglinskaya, O, Zykov, K, Dopudja Pantic, V, Nadaskic, R, Nestorovic, B, Skodric Trifunovic, V, Stojanovic, A, Vukcevic, M, Vujic, T, Mitic Milikic, M, Banovcin, P, Horvathova, H, Karako, P Sr, Plutinsky, J, Pribulova, E, Szarazova, M, Zlatos, A, Adams, L, Badat, A, Bassa, A, Breedt, J, Bruning, A, Ellis, Gc, Emanuel, S, Fouche, Lf, Fulat, Ma, Gani, M, Ismail, Ms, Jurgens, Jc, Nell, H, Nieuwoudt, G, Noor, F, Bolliger, Ct, Puterman, As, Siddique, N, Trokis, Js, Vahed, Ya, Van Der Berg BJ, Van der Linden, M, Van Zyl, L, Visser, Ss, Antépara Ercoreca, I, Arnedillo Muñoz, A, Barbe Illa, F, Barreiro López, B, Blanco Aparicio, M, Boada Valmaseda, A, Bosque García, M, Bustamante Ruiz, A, Carretero Anibarro, P, Del Campo Matias, F, Echave-Sustaet, Jm, Espinosa de los Monteros Garde MJ, Garcia Hernandez GM, López Viña, A, Lores Obradors, L, Luengo Planas MT, Monsó Molas, E, Navarro Dourdil, A, Nieto García AJ, Perpina Tordera, M, Picado Valles, C, Rodriguez Alvarez Mdel, M, Saura Vinuesa, A, Serra Batlles, J, Soler Sempere MJ, Toran Montserrat, P, Valdés Cuadrado LG, Villasante Fernandez-Montes, C, Cheng, Sl, Chern, Jh, Chiu, Mh, Chung, Cl, Lai, Rs, Lin, Ck, Liu, Yc, Wang, Cc, Wei, Yf, Amer, L, Berenfus, Vi, Besh, L, Duka, Kd, Fushtey, Im, Garmash, N, Dudnyk, O, Godlevska, O, Vlasenko, Ma, Hospodarskyy, I, Iashyna, L, Kaladze, M, Khvelos, Si, Kostromina, Vp, Krakhmalova, O, Kryuchko, T, Kulynych, Ov, Krasko, Mp, Levchenko, O, Litvinova, T, Panina, Ss, Pasiyeshvili, Lm, Prystupa, Ln, Romaniuk, Li, Sirenko, I, Synenko, Vi, Vynnychenko, Lb, Yatsyshyn, Ri, Zaitsev, I, Zhebel, V, Zubarenko, O, Arthur, Cp, Brown, V, Burhan, H, Chaudhuri, R, Collier, D, Barnes, Nc, Davies, Ej, Ellery, A, Kwok, S, Lenney, W, Nordstrom, M, Pandya, Hc, Parker, Iw, Rajakulasingam, K, Seddon, P, Sharma, R, Thomas, Ec, Wakeling, Ja, Abalos-Galito, M, Abboy, C, Abreu, E, Ackerman, If, Acosta, Ia, Adaoag, Aa, Ahmed, M, Ali, Mi, Allen, Dr, Allen GG Jr, Diogo, Jj, Allison, Dc, Alwine, Lk, Apaliski, Sj, Arastu, Rs, Arora, Cm, Auerbach, D, Azzam, Sj, Badar FL 3rd, Baker, Jw, Barasch, Jp, Barber, Ma, Bardinas-Rodriguez, R, Barreiro, Tj, Baumbach, Rr, Baur, Ce, Baxter, Bs, Beach, Jl, Beasley, Rl, Beavins, Je, Beliveau, Wj, Benbow, Mj, Bennett, Nl, Bennett, Rl, Bernal, H, Bernstein, Di, Blaiss, Ms, Blumenthal, Kw, Boas, Sr, Borders, Jl, Boscia, Ja, Boulware, Wn, Bowling, Bt, Brabec, Ba, Bramlet, Dg, Figueroa, Dp, Brautigam, Df, Brownell, Jm, Bruce, Tr, Call, Rs, Campbell, Ca, Canaan, Ya, Cannon, Df, Carpio, Jm, Cathcart, Ws, Cevallos, Jp, Chauhan, Av, Chuang, Rb, Chevalier, D, Christensen, J, Christensen, Ta, Christina, Mo, Chrzanowski, Rr, Civitarese, Fa, Clark, Jp, Clifford, Dp, Lapidus, Rj, Coggi, Ja, Lenz, Jj, Cohen, Kr, Collins, Bg, Collins, H, Comellas, A, Condit, J, Cordasco EM Jr, Corder, Cn, Covar, Ra, Coverston, Kd, Croce, Sa, Cruz, H, Curtis, Ct, Daftary, Pk, Dalan, D, Dalawari, Sp, Daly, Wc, Davis, Kc, Dawes, Kw, Decotiis, Ba, Deluca, Rf, Desantis, Dm, De Valle OL, Diaz, Jl, Diaz, Jd, Dice, Jp, Elizalde, A, Hosler, Mr, Dixon, C, Dobkin, La, Dobrusin, Rs, Dransfield, Mt, Ebbeling, Wl, Edwards, Jd, Elacion, Jm, Elkayam, D, Ellison, Wt, Elsen, Jr, Engel, Lr, Ensz, Dj, Ericksen, Cl, Ervin, Je, Fang, C, Abrahamian, F, Farrah, Vb, Field, Jd, Fishman, Hj, Florea, R, Nayyar, S, Focil, A, Focauld, F, Franco MA Jr, Frandsen, Br, Ganti, K, Garcia, Fl, Lee, Wm, Garscadden, Ag, Gatti, Ea, Gellady, Am, George, Ar, Gibbon, Gw, Gleason, Gp, Goldberg, P, Goldstein, Mf, Gonzalez, Ge, Gower, Rg, Grande, Ja, Gregory, D, Grubb, Sd, Guthrie, Rp, Haas, Ta, Haft, Ks, Hajal, R, Hammond, Gd, Hansel, Nn, Hansen, Vr, Harris, Af, Hartman, An, Harvey, Rr, Hazan-Steinberg, S, Headley, Dm, Heigerick, Gc, Heller, Bn, Hendrix, El, Herrod, Jn, Hewitt, Mj, Hines, Rl, Hirdt, Ap, Hirschfield, Ja, Hoffman, Ks, Hogan, Ad, Howland, Wc, Hsu, Cc, Hsu, Fj, Hubbard, Wm, Hudson, Jd, Huffman, C, Hussain, M, Ioachimescu, Oc, Ismail, Ym, Jaffrani, Na, Jiang, N, Jones, Sw, Jordan, Rs, Joshi, Ke, Kaashmiri, Mw, Kalafer, M, Kamdar, Ba, Kanuga, Jg, Kao, Nl, Karetzky, M, Katsetos, Jc, Kay, Js, Kimmel, Ma, Kimura, Sh, Kingsley, Jk, Mahmood, Sm, Subich, Dc, Kirstein, Jl, Kleerup, Ec, Klein, Rm, Koh, Dw, Kohli, N, Koura, Fa, Kovacs, Sp, Kratzer, J, Kreit, Ci, Kreutter, Fm, Kubicki, Tm, Labuda, Jm, Latorre, Aj, Lara, Mm, Lechin, Ae, Lee, Jj, Lee, Md, Lentnek, Al, Lesh, Kw, Levins, Pf, Anspach, Rb, Levinsky, Dm, Lillestol, Mj, Lim, H, Livezey, Md, Lloyd-Turney, Cw, Lockey, Rf, Long, Ra, Lynch, Mj, Macgillivray, Bk, Mahadevan, Kp, Makam, Sk, Maloney, Mj, Mapel, D, Margolis, Bd, Margulies, J, Martin, Ef, Martin, Ee, Mascolo, M, Mataria, H, Sunbuli, M, Mathur, Rn, Mattar, Pn, Maynard, Km, Maynard, N, Mccormick, B, Mcelya, M, Mcevoy, Ce, Mckenzie, Wc, Medwedeff, Le, Mehta, Kd, Melamed, Ir, Meli, Jv, Merrick, Bh, Meyers, Pj, Miller, Bt, Minton, Sm, Miranda, Fg, Mohar, De, Montenegro, Ch, Morris, Fa, Morrison, Bs, Moss, Mh, Munoz, F, Naini, Gr, Nakamura, Ct, Naseeruddin, S, Nassim, C, Navazo, Lj, Nissim, Je, Norman, D, Oberoi, Ms, O'Connor, Tm, Offenberger, J, Orr, Rr, Osea, Ea, Paine, Wj, Rasmussen, Nl, Palatnik, M, Pangtay, D, Panuto, Ja, Patel, M, Perera, Ms, Perez, A, Peters PH Jr, Pimentel SM Jr, Pluto, Tm, Pollock, Mt, Posner, Ls, Pritchard, Jc, Pudi, Kk, Puig, Cm, Qaqundah, Py, Radbill, Mk, Rahman, St, Raikhel, M, Raissy, Hh, Ramstad, Ds, Ranasinghe, Es, Rangel, Os, Rapo, Se, Raschal, Sp, Reddy, Dg, Rehman, Sm, Reyes, Sr, Rhodes, Rb, Riffer, E, Rihal, Ps, Riley ED 4th, Rodriguez, Dh, Rogers, Cm, Rohlf, Jl, Romeu, H, Roney, Cw, Ronsick, So, Rosen, Jb, Rowe, Ms, Ruoff, Ge, Ryan, Eh, Saff, Rh, Saini, N, Anand, S, Balakrishnan, K, Samuels, Bs, Samuelson, Rj, Saniuk, Rj, Sargeant, Wo, Saunders, Mk, Saway, W, Scarupa, Md, White, Mv, Schear, Mj, Schwarz, Cm, Scott, Rb, Segall, N, Seibert, Af, Seidmeyer, V, Seidner, Mr, Seifer, Fd, Serje, J, Shah, Ms, Shah, Sb, Shapero, Pa, Shearer, Sd, Sheikh, Sq, Shepherd, Ts, Sher, Er, Sher, Ld, Short, Bh, Silas, Pe, Alvey, Jc, Silverfield, Jc, Simon, Sj, Sitar, S, Skoner, Dp, Smallow, Sa, Smart, Ba, Smith, Ca, Smith, Ke, Smith, Sk, Snyders, Gc, Soong, W, Soufer, J, Spangenthal, S, Stahlman, Je, Steele, Lg, Stegemoller, Rk, Stocks, J, Storms, Ww, Suen, J, Surowitz, Rz, Swauger, Jr, Taber, La, Tan, Ae, Pratt, Se, Tanus, T, Tarpay, Mm, Tarshis, Ga, Tenney, Jw, Tilghman, Kg, Trevino, Me, Troyan, Be, Twiddy, Sk, Updegrove, Jd, Urval, Kr, Uusinarkaus, Kt, Vaela, R, Van Cleeff, M, Varano, S, Vo, Qd, Wainz, Rj, Wald, Ja, Wall, Sj, Wasserman, Rl, Weinstein, Dl, Welker, Ja, Wellmon, B 2nd, Wells, T, Wenocur, Hs, Williams, Dl, Williams, Sl, Win, Ph, Wingo, Td, Wisman PP Jr, Wyszomierski, Da, Yamada, Hm, Yarows, S, Yunger TM Jr, Ziering, Rw., the AUSTRI Investigators, Stempel, D., Raphiou, I., Kral, K., Yeakey, A., Emmett, A., Prazma, C., Buaron, K., and Pascoe, S. Scichilone N tra i collaboratori

Subjects
Male, asthma, serious events, fluticasone, salmeterol, AUSTRI, Exacerbation, Intention to Treat Analysi, INHALED CORTICOSTEROIDS, Severity of Illness Index, law.invention, 0302 clinical medicine, Randomized controlled trial, law, immune system diseases, Ús terapèutic, Broncodilatadors, 030212 general & internal medicine, Child, Fluticasone, RISK, ACTING BETA-AGONISTS, EXACERBATIONS, METAANALYSIS, MORTALITY, SAFETY, DEATH, FDA, Medicine (all), Hazard ratio, General Medicine, Bronchodilator agents, Middle Aged, Fluticasone-Salmeterol Drug Combination, Bronchodilator Agents, Intention to Treat Analysis, Anesthesia, Female, Salmeterol, medicine.drug, Human, Adult, medicine.medical_specialty, Adolescent, Settore MED/10 - Malattie Dell'Apparato Respiratorio, Fluticasone propionate, 03 medical and health sciences, Double-Blind Method, Internal medicine, Administration, Inhalation, medicine, Humans, Asma, Bronchodilator Agent, Asthma, Aged, Proportional Hazards Models, business.industry, Therapeutic use, medicine.disease, respiratory tract diseases, 030228 respiratory system, Fluticasone Propionate, Salmeterol Xinafoate Drug Combination, Proportional Hazards Model, business
Abstract

BACKGROUND The safe and appropriate use of long-acting beta-agonists (LABAs) for the treatment of asthma has been widely debated. In two large clinical trials, investigators found a potential risk of serious asthma-related events associated with LABAs. This study was designed to evaluate the risk of administering the LABA salmeterol in combination with an inhaled glucocorticoid, fluticasone propionate. METHODS In this multicenter, randomized, double-blind trial, adolescent and adult patients (age, ≥12 years) with persistent asthma were assigned to receive either fluticasone with salmeterol or fluticasone alone for 26 weeks. All the patients had a history of a severe asthma exacerbation in the year before randomization but not during the previous month. Patients were excluded from the trial if they had a history of lifethreatening or unstable asthma. The primary safety end point was the first serious asthma-related event (death, endotracheal intubation, or hospitalization). Noninferiority of fluticasone–salmeterol to fluticasone alone was defined as an upper boundary of the 95% confidence interval for the risk of the primary safety end point of less than 2.0. The efficacy end point was the first severe asthma exacerbation. RESULTS Of 11,679 patients who were enrolled, 67 had 74 serious asthma-related events, with 36 events in 34 patients in the fluticasone–salmeterol group and 38 events in 33 patients in the fluticasone-only group. The hazard ratio for a serious asthmarelated event in the fluticasone–salmeterol group was 1.03 (95% confidence interval [CI], 0.64 to 1.66), and noninferiority was achieved (P = 0.003). There were no asthma-related deaths; 2 patients in the fluticasone-only group underwent asthmarelated intubation. The risk of a severe asthma exacerbation was 21% lower in the fluticasone–salmeterol group than in the fluticasone-only group (hazard ratio, 0.79; 95% CI, 0.70 to 0.89), with at least one severe asthma exacerbation occurring in 480 of 5834 patients (8%) in the fluticasone–salmeterol group, as compared with 597 of 5845 patients (10%) in the fluticasone-only group (P

Published
2016

9. Inflammatory endotypes of chronic rhinosinusitis based on cluster analysis of biomarkers

Author

Elina Toskala, Glenis Scadding, Thibaut Van Zele, Claus Bachert, Peter Tomassen, Valerie J. Lund, Natalie De Ruyck, Peter Hellings, Lars-Olaf Cardell, Xiangdong Wang, Agnieszka Olszewska-Ziąber, Joaquim Mullol, Wytske Fokkens, Heidi Olze, Cornelis M. van Drunen, Gabriele Holtappels, Valérie Hox, U Förster-Ruhrmann, Julia Arebro, Luo Zhang, Griet Vandeplas, Marek L. Kowalski, and Ear, Nose and Throat

Subjects
Male, Endotype, Immunoglobulin E, Enterotoxins, 0302 clinical medicine, Medicine and Health Sciences, Cluster Analysis, Immunology and Allergy, Nasal polyps, SINUS DISEASE, 030223 otorhinolaryngology, Sinusitis, Rhinitis, Principal Component Analysis, Eosinophil cationic protein, nasal polyps, biology, ASSOCIATION, endotypes, Cytokines, Female, medicine.symptom, TH22 CELLS, Adult, Staphylococcus aureus, EUROPE, Bacterial Toxins, Immunology, Inflammation, PHENOTYPES, 03 medical and health sciences, medicine, otorhinolaryngologic diseases, Humans, IGE, Peroxidase, Asthma, IDENTIFICATION, business.industry, Case-control study, asthma, medicine.disease, Chronic rhinosinusitis, 030228 respiratory system, inflammation, Case-Control Studies, Chronic Disease, biology.protein, business, Biomarkers, cluster analysis
Abstract

Background: Current phenotyping of chronic rhinosinusitis (CRS) into chronic rhinosinusitis with nasal polyps (CRSwNP) and chronic rhinosinusitis without nasal polyps (CRSsNP) might not adequately reflect the pathophysiologic diversity within patients with CRS. Objective: We sought to identify inflammatory endotypes of CRS. Therefore we aimed to cluster patients with CRS based solely on immune markers in a phenotype-free approach. Secondarily, we aimed to match clusters to phenotypes. Methods: In this multicenter case-control study patients with CRS and control subjects underwent surgery, and tissue was analyzed for IL-5, IFN-gamma, IL-17A, TNF-alpha, IL-22, IL-1 beta, IL-6, IL-8, eosinophilic cationic protein, myeloperoxidase, TGF-beta 1, IgE, Staphylococcus aureus enterotoxin-specific IgE, and albumin. We used partition-based clustering. Results: Clustering of 173 cases resulted in 10 clusters, of which 4 clusters with low or undetectable IL-5, eosinophilic cationic protein, IgE, and albumin concentrations, and 6 clusters with high concentrations of those markers. The group of IL-5-negative clusters, 3 clusters clinically resembled a predominant chronic rhinosinusitis without nasal polyps (CRSsNP) phenotype without increased asthma prevalence, and 1 cluster had a T(H)17 profile and had mixed CRSsNP/CRSwNP. The IL-5-positive clusters were divided into a group with moderate IL-5 concentrations, a mixed CRSsNP/CRSwNP and increased asthma phenotype, and a group with high IL-5 levels, an almost exclusive nasal polyp phenotype with strongly increased asthma prevalence. In the latter group, 2 clusters demonstrated the highest concentrations of IgE and asthma prevalence, with all samples expressing Staphylococcus aureus enterotoxin-specific IgE. Conclusion: Distinct CRS clusters with diverse inflammatory mechanisms largely correlated with phenotypes and further differentiated them and provided a more accurate description of the inflammatory mechanisms involved than phenotype information only.

Published
2016

10. The GALEN rhinosinusitis cohort: chronic rhinosinusitis with nasal polyps affects health-related quality of life.

Author

Khan, Asif, Thi Minh Thao Huynh, Vandeplas, Griet, Joish, Vijay N., Mannent, Leda P., Tomassen, Peter, van Zele, Thibaut, Cardell, Lars-Olaf, Arebro, Julia, Olze, Heidi, Förster-Ruhrmann, Ulrike, Kowalski, Marek L., Olszewska-Ziąber, Agnieszka, Fokkens, Wytske, van Drunen, Cornelis, Mullol, Joaquim, Alobid, Isam, Hellings, Peter W., Hox, Valérie, and Toskala, Elina

Published
2019
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11. The Global Allergy and Asthma European Network (GALEN) rhinosinusitis cohort: a large European cross-sectional study of chronic rhinosinusitis patients with and without nasal polyps.

Author

Khan, Asif, Vandeplas, Griet, Thi Minh Thao Huynh, Joish, Vijay N., Mannent, Leda, Tomassen, Peter, Van Zele, Thibaut, Cardell, Lars-Olaf, Arebro, Julia, Olze, Heidi, Förster-Ruhrmann, Ulrike, Kowalski, Marek L., Olszewska-Ziąber, Agnieszka, Holtappels, Gabriële, De Ruyck, Natalie, van Drunen, Cornelis, Mullol, Joaquim, Hellings, Peter W., Hox, Valerie, and Toskala, Elina

Published
2019
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12. Impaired virus replication and decreased innate immune responses to viral infections in nasal epithelial cells from patients with allergic rhinitis

Author

Głobińska, A, primary, Pawełczyk, M, additional, Piechota-Polańczyk, A, additional, Olszewska-Ziąber, A, additional, Moskwa, S, additional, Mikołajczyk, A, additional, Jabłońska, A, additional, Zakrzewski, P K, additional, Brauncajs, M, additional, Jarzębska, M, additional, Taka, S, additional, Papadopoulos, N G, additional, and Kowalski, M L, additional

Published
2016
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13. Clinical benefits of aspirin desensitization in patients with nonsteroidal anti-inflammatory drug exacerbated respiratory disease are not related to urinary eicosanoid release and are accompanied with decreased urine creatinine

Author

Makowska, Joanna S., primary, Olszewska-Ziąber, Agnieszka, additional, Bieńkiewicz, Barbara, additional, Lewandowska-Polak, Anna, additional, Kurowski, Marcin, additional, Woźniakowski, Bartłomiej, additional, Rotkiewicz, Arkadiusz, additional, and Kowalski, Marek L., additional

Published
2016
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15. The ‘GA²LEN Sinusitis Cohort’: an introduction

Author

Vandeplas, Griet, primary, Khan, Asif, additional, Huynh, Thi Minh Thao, additional, Tomassen, Peter, additional, Zele, Thibaut, additional, Cardell, Lars‐Olaf, additional, Arebro, Julia, additional, Olze, Heidi, additional, Foerster, Ulrike, additional, Kowalski, Marek Leszek, additional, Olszewska‐Ziąber, Agnieszka, additional, Fokkens, Wytske, additional, Drunen, Cornelis, additional, Mullol, Joaquim, additional, Hellings, Peter, additional, Hox, Valérie, additional, Toskala, Elina, additional, Scadding, Glenis, additional, Lund, Valerie, additional, and Bachert, Claus, additional

Published
2015
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16. The ‘GA²LEN Sinusitis Cohort’: an introduction

Author

Griet Vandeplas, Asif Khan, Agnieszka Olszewska-Ziąber, Elina Toskala, Marek L. Kowalski, Peter Tomassen, Claus Bachert, Heidi Olze, Cornelis M. van Drunen, Joaquim Mullol, Valerie J. Lund, Ulrike Foerster, Thi Minh Thao Huynh, Julia Arebro, Wytske Fokkens, Thibaut Van Zele, Peter Hellings, Glenis Scadding, Valérie Hox, and Lars-Olaf Cardell

Subjects
Pulmonary and Respiratory Medicine, medicine.medical_specialty, Allergy, business.industry, Chronic rhinosinusitis, Immunology, Alternative medicine, Disease, medicine.disease, Internal medicine, Cohort, medicine, Immunology and Allergy, Oral Presentation, Sinusitis, business, Asthma
Abstract

Background The Global Allergy and Asthma European Network (GALEN) is a network of the leading European allergy clinical and research facilities and the GALEN Sinusitis Cohort is a database within this network. The aim of this cohort is to intensify research on rhinosinusitis phenoand endotypes, thus differentiating chronic rhinosinusitis (CRS) into smaller disease entities based on clinical, biological, and patient-reported outcomes.

Published
2015

17. Impaired virus replication and decreased innate immune responses to viral infections in nasal epithelial cells from patients with allergic rhinitis.

Author

Głobińska, A., Pawełczyk, M., Piechota‐Polańczyk, A., Olszewska‐Ziąber, A., Moskwa, S., Mikołajczyk, A., Jabłońska, A., Zakrzewski, P. K., Brauncajs, M., Jarzębska, M., Taka, S., Papadopoulos, N. G., and Kowalski, M. L.

Subjects
VIRAL replication, NATURAL immunity, EPITHELIAL cells, ALLERGIC rhinitis, PARAINFLUENZA viruses
Abstract

The aim of this study was to assess the immune response to parainfluenza virus type 3 (PIV3), rhinovirus 1B (RV1B) and intracellular Toll-like receptors (TLR) agonists in nasal epithelial cells (NECs) from patients with allergic rhinitis and healthy controls. NECs were obtained from eight patients with allergic rhinitis (AR) and 11 non-atopic healthy controls (HC) by nasal scraping, grown to confluence and exposed to PIV3, RV1B infection or TLR-3 and TLR-7/8 agonists. Interferon (IFN)-λ1, IFN-α, IFN-β and regulated on activation, normal T expressed and secreted (RANTES) release into the cell culture supernatants was assessed at 8, 24 and 48 h upon infection or 8 and 24 h after stimulation with poly(I:C) and R848. mRNA levels of IFNs, RANTES, interferon regulatory transcription factor (IRF)3, IRF7 and viral gene copy number were determined using real-time polymerase chain reaction (RT-PCR). PIV3 but not RV1B replication 48 h after infection was significantly lower ( P < 0·01) in NECs from AR patients compared to HC. PIV3 infection induced significantly less IFN-λ1 (both protein and mRNA) in NECs from AR compared to HC. IFN-β mRNA expression and RANTES protein release and mRNA expression tended to be smaller in AR compared HC cells in response to both viruses. Stimulation with TLR-3 agonist [poly (I:C)] induced similar IFN-λ1 and RANTES generation in AR and HC subjects. Viral infections in NECs induced IRF7 expression, which correlated with IFN and RANTES expression. These data suggest that virus proliferation rates and the immune response profile are different in nasal epithelial cells from patients with allergic rhinitis compared to healthy individuals. [ABSTRACT FROM AUTHOR]

Published
2017
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19. 142 The Immune Response Against Respiratory Pathogens in Patients with Chronic Rhinosinusitis/Nasal Polyps and Asthma with or without Sensitivity to Aspirin

Author

Marzanna Jarzębska, Agnieszka Olszewska-Ziąber, and Marek L. Kowalski

Subjects
Pulmonary and Respiratory Medicine, Aspirin, business.industry, Oral Abstract Session, Immunology, Inflammation, respiratory system, medicine.disease, Abstracts of the XXII World Allergy Congress, respiratory tract diseases, Respiratory pathogens, Immune system, medicine.anatomical_structure, medicine, otorhinolaryngologic diseases, Immunology and Allergy, Nasal polyps, In patient, medicine.symptom, business, Sensitization, Asthma, medicine.drug
Abstract

Background Viral and bacterial infections can modulate the ongoing inflammation in both upper and lower airways of patients with chronic rhinosinusitis with nasal polyps (CRS/NP) and asthma. It was not clear if the protective immune response to pathogens may differ depending on the disease severity. Object: To compare serum IgG immune response against respiratory pathogens in patients with chronic airway disease (CRS/NP and asthma) with and without sensitivity to aspirin, and to refer the sensitization to severity of chronic rhinosinusitis. Methods We recruited 73 patients with CRS/NP and asthma with (43 patients) and without (30 patients) hypersensitivity to aspirin. The extent of mucosal hypertrophy in paranasal sinuses was assessed by CT scans and the sense of smell was valuated with “sniffing smell” test. Serum IgG immunoglobulin levels against respiratory pathogens: Respiratory Syncytial Virus (RSV), Adenowirus (ADV), Parainfluenza virus (PIV) and Mycoplasma pneumoniae were determined by ELISA. Results Patients with ASA-hypersensitivity had history of significantly more nasal polypectomies (P = 0.002), lower smell test score (P = 0.03) and higher mean paranasal CT score (P = 0.03) as compared to ASA-tolerant patients, reflecting higher severity of the upper airway disease. The percentage of positive serological testing to respiratory pathogens was very high in the whole group of patients with CRS/NP and asthma (RSV, 95.8%; ADV, 95.9%; PIV, 84.9% and Mycoplasma pneumonieae, 100% patients) without any difference between ASA-sensitive and ASA-tolerant subjects. Patients with ASA-sensitivity had significantly lower concentrations of PIV- specific IgG (mean 188.67 ± 34.46 U/mL versus 207.56 ± 30.036 U/mL; P < 0.04) as compared to ASA-tolerant subjects. There was a significant trend (P < 0.048) for lower PIV–specific IgG concentrations with increased number of polypectomies. No correlation of IgG immunoglobulin concentrations for other pathogens with the number of polypectomies, paranasal sinuses CT score or presences of smell were observed. Conclusions Patients with CRS/NP and asthma had high frequency of IgG immunoglobulin against common respiratory pathogens. Serum IgG immune response to paramyxoviruses may be related to the recurrence of nasal polyps and the presence of aspirin sensitivity.

Published
2012

21. Enhanced inhibition of nasal epithelial cell repair by innate stimulation in patients with allergic rhinitis.

Author

LEWANDOWSKA-POLAK, ANNA, BRAUNCAJS, MAŁGORZATA, JARZĘBSKA, MARZANNA, OLSZEWSKA-ZIĄBER, AGNIESZKA, MAKOWSKA, JOANNA, and KOWALSKI, MAREK L.

Subjects
*EPITHELIAL cells, *ALLERGIC rhinitis, *EPITHELIUM, *NASAL mucosa, *MICROBIAL products, *TOLL-like receptors, *WOUND healing
Abstract

Introduction. Impaired repair of airway epithelium may lead to persistence of inflammation and remodelling. Regeneration of injured epithelium is a complex phenomenon and the role of toll-like receptors (TLRs) and respiratory virus products in this process have not been established. Aim of the study. In this study we aimed to test if wound repair in nasal epithelial cells is modulated by microbial products and if this process was different in patients with allergic rhinitis and in healthy subjects. Materials and methods. Injured human nasal epithelial cells (hNECs) monolayers were incubated with the toll-like receptors agonists: poly (I:C) and lipopolisacharide (LPS); allergen Der p1, and supernatants from virus-infected epithelial cells. Regeneration of injured epithelium was assessed by measuring changes in the area of epithelial damage. Results. Addition of either poly (I:C) or LPS induced a dose dependant inhibition of wound repair in hNECs monolayers. Supernatants from RV1b-infected cells decreased epithelial cell regeneration after mechanical injury only in allergic patients. At baseline conditions the dynamics of epithelial repair was similar in allergic and non-allergic epithelium. However, inhibitory effects of innate stimuli on epithelial repair was stronger in patients with allergic rhinitis as compared to healthy individuals. Conclusions. This study showed that microbial products may affect regeneration of the nasal epithelium, and allergic patients are more susceptible to suppression of epithelial regeneration. [ABSTRACT FROM AUTHOR]

Published
2019

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