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10 results on '"Haimerl, Pascal"'

1. Macrophages acquire a TNF-dependent inflammatory memory in allergic asthma

Author

Lechner, Antonie, Henkel, Fiona D.R., Hartung, Franziska, Bohnacker, Sina, Alessandrini, Francesca, Gubernatorova, Ekaterina O., Drutskaya, Marina S., Angioni, Carlo, Schreiber, Yannick, Haimerl, Pascal, Ge, Yan, Thomas, Dominique, Kabat, Agnieszka M., Pearce, Edward J., Ohnmacht, Caspar, Nedospasov, Sergei A., Murray, Peter J., Chaker, Adam M., Schmidt-Weber, Carsten B., and Esser-von Bieren, Julia

Published
2022
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3. Extracellular vesicle miRNAs drive aberrant macrophage responses in NSAID‐exacerbated respiratory disease.

Author

Hartung, Franziska, Haimerl, Pascal, Schindela, Sonja, Mussack, Veronika, Kirchner, Benedikt, Henkel, Fiona D. R., Bernhardt, Ulrike, Zissler, Ulrich M., Santarella‐Mellwig, Rachel, Pfaffl, Michael, Schmidt‐Weber, Carsten B., Chaker, Adam M., and Esser‐von Bieren, Julia

Subjects
*EXTRACELLULAR vesicles, *RESPIRATORY diseases, *MICRORNA, *MACROPHAGE activation, *NASAL tumors, *MACROPHAGES
Abstract

Background: Extracellular vesicles (EVs) have been implicated in the pathogenesis of asthma, however, how EVs contribute to immune dysfunction and type 2 airway inflammation remains incompletely understood. We aimed to elucidate roles of airway EVs and their miRNA cargo in the pathogenesis of NSAID‐exacerbated respiratory disease (N‐ERD), a severe type 2 inflammatory condition. Methods: EVs were isolated from induced sputum or supernatants of cultured nasal polyp or turbinate tissues of N‐ERD patients or healthy controls by size‐exclusion chromatography and characterized by particle tracking, electron microscopy and miRNA sequencing. Functional effects of EV miRNAs on gene expression and mediator release by human macrophages or normal human bronchial epithelial cells (NHBEs) were studied by RNA sequencing, LC–MS/MS and multiplex cytokine assays. Results: EVs were highly abundant in secretions from the upper and lower airways of N‐ERD patients. N‐ERD airway EVs displayed profoundly altered immunostimulatory capacities and miRNA profiles compared to airway EVs of healthy individuals. Airway EVs of N‐ERD patients, but not of healthy individuals induced inflammatory cytokine (GM‐CSF and IL‐8) production by NHBEs. In macrophages, N‐ERD airway EVs exhibited an impaired potential to induce cytokine and prostanoid production, while enhancing M2 macrophage activation. Let‐7 family miRNAs were highly enriched in sputum EVs from N‐ERD patients and mimicked suppressive effects of N‐ERD EVs on macrophage activation. Conclusion: Aberrant airway EV miRNA profiles may contribute to immune dysfunction and chronic type 2 inflammation in N‐ERD. Let‐7 family miRNAs represent targets for correcting aberrant macrophage activation and mediator responses in N‐ERD. [ABSTRACT FROM AUTHOR]

Published
2024
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5. Macrophages acquire a TNF-dependent inflammatory memory in allergic asthma

Author

Hartung, Franziska, primary, Lechner, Antonie, additional, Henkel, Fiona, additional, Bohnacker, Sina, additional, Alessandrini, Francesca, additional, Gubernatorova, Ekaterina O., additional, Drutskaya, Marina S., additional, Angioni, Carlo, additional, Schreiber, Yannick, additional, Haimerl, Pascal, additional, Ge, Yan, additional, Thomas, Dominique, additional, Ohnmacht, Caspar, additional, Nedospasov, Sergei A., additional, Murray, Peter J., additional, Chaker, Adam M., additional, Schmidt-Weber, Carsten B., additional, and Esser-Von Bieren, Julia, additional

Published
2022
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6. An anti-inflammatory eicosanoid switch mediates the suppression of type-2 inflammation by helminth larval products

Author

de los Reyes Jiménez, Marta, primary, Lechner, Antonie, additional, Alessandrini, Francesca, additional, Bohnacker, Sina, additional, Schindela, Sonja, additional, Trompette, Aurélien, additional, Haimerl, Pascal, additional, Thomas, Dominique, additional, Henkel, Fiona, additional, Mourão, André, additional, Geerlof, Arie, additional, da Costa, Clarissa Prazeres, additional, Chaker, Adam M., additional, Brüne, Bernhard, additional, Nüsing, Rolf, additional, Jakobsson, Per-Johan, additional, Nockher, Wolfgang A., additional, Feige, Matthias J., additional, Haslbeck, Martin, additional, Ohnmacht, Caspar, additional, Marsland, Benjamin J., additional, Voehringer, David, additional, Harris, Nicola L., additional, Schmidt-Weber, Carsten B., additional, and Esser-von Bieren, Julia, additional

Published
2020
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7. Multi-omics characterization of NSAID-exacerbated respiratory disease: Altered lipid metabolism and macrophage activation

Author

Schmidt-Weber, Carsten (Prof. Dr.), Feige, Matthias (Prof. Dr.), Haimerl, Pascal, Schmidt-Weber, Carsten (Prof. Dr.), Feige, Matthias (Prof. Dr.), and Haimerl, Pascal

Abstract

Treatment options for chronic inflammatory airway diseases are limited due to an incomplete understanding of the underlying pathomechanisms. In this thesis, metabolic- and immune cell profiles of patients with NSAID-exacerbated respiratory disease (N-ERD), a severe type 2 inflammatory condition, were characterized by multi-omics approaches. N-ERD macrophages displayed a persistent, pro-inflammatory phenotype, which was associated with local and systemic lipid metabolism alterations. Our study suggests that pro-inflammatory macrophage reprogramming is a pathomechanism of N-ERD., Die Therapiemöglichkeiten für chronisch-entzündliche Atemwegserkrankungen sind aufgrund eines unvollständigen mechanistischen Verständnisses limitiert. In dieser Studie wurden metabolische und immunologische Profile von Patienten mit Samter Trias (engl. N-ERD), einer besonders schweren Atemwegsentzündung des Typs 2, mittels Multi-Omics-Ansätzen charakterisiert. Unsere Analysen zeigen einen (lokal und systemisch) veränderten Lipidstoffwechsel und eine fehlgeleitete Aktivierung von Makrophagen als mögliche Pathomechanismen von N-ERD auf.

Published
2020

8. House dust mite drives pro‐inflammatory eicosanoid reprogramming and macrophage effector functions

Author

Henkel, Fiona D. R., primary, Friedl, Antonie, additional, Haid, Mark, additional, Thomas, Dominique, additional, Bouchery, Tiffany, additional, Haimerl, Pascal, additional, de los Reyes Jiménez, Marta, additional, Alessandrini, Francesca, additional, Schmidt‐Weber, Carsten B., additional, Harris, Nicola L., additional, Adamski, Jerzy, additional, and Esser‐von Bieren, Julia, additional

Published
2018
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9. Abstracts from the 11th Symposium on Experimental Rhinology and Immunology of the Nose (SERIN 2017)

Author

Gracia, Ibon Eguiluz, primary, Rondón, Carmen, additional, Campo, Paloma, additional, Prieto, Ana, additional, Mayorga, Lina, additional, Galindo, Luisa, additional, Molina, Ana, additional, Blanca, Miguel, additional, Torres, Maria Jose, additional, Morikawa, Taiyo, additional, Fukuoka, Ayumi, additional, Matsushita, Kazufumi, additional, Fujieda, Shigeharu, additional, Yoshimoto, Tomohiro, additional, Iwasaki, Naruhito, additional, Smulders, Tamar, additional, Van Egmond, Danielle, additional, Van Drunen, Kees, additional, Van Der Schee, Marc, additional, Beule, Achim Georg, additional, Berings, Margot, additional, Jult, Anton, additional, Vermeulen, Hanne, additional, De Ruyck, Natalie, additional, Derycke, Lara, additional, Ucar, Hakan, additional, Ghekiere, Philip, additional, Temmerman, Robin, additional, Ellis, John, additional, Bachert, Claus, additional, Lambrecht, Bart, additional, Dullaers, Melissa, additional, Gevaert, Philippe, additional, Arasi, Stefania, additional, Perna, Serena, additional, Resch, Yvonne, additional, Lupinek, Christian, additional, Chen, Kuan-Wei, additional, Vrtala, Susanne, additional, Valenta, Rudolf, additional, Matricardi, Paolo Maria, additional, Gonçalves, Ivânia, additional, Jacinto, Tiago, additional, Amaral, Rita, additional, Pereira, Ana M., additional, Araújo, Luís M., additional, Couto, Mariana, additional, Fonseca, João A., additional, Stjarne, Par, additional, Kaulsay, Ranbir, additional, Pohl, Wolfgang, additional, Plaza, Maria Carmen, additional, Prieto, Ana Maria, additional, Mayorga, Cristobalina, additional, Herknerova, Magdalena, additional, Wang, Tengchin, additional, Wu, Chiejun, additional, Kilimajer, Jonathan, additional, Pujols, Laura, additional, Roca-Ferrer, Jordi, additional, Callejas, Borja, additional, Fuentes-Prado, Mireya, additional, Perez-Gonzalez, Maria, additional, Alobid, Isam, additional, Valero, Antonio, additional, Picado, Cesar, additional, Murray, Ruth, additional, Mullol, Joaquim, additional, Steelant, Brecht, additional, Martens, Katleen, additional, Boeckxstaens, Guy, additional, Seys, Sven F., additional, Hellings, Peter W., additional, Biggs, Timothy C., additional, Hayes, Stephen M., additional, Harries, Philip G., additional, Pender, Sylvia, additional, Salib, Rami J., additional, Kim, Jean, additional, Lee, Hyun Sil, additional, Kalogjera, Livije, additional, Vrkic, Nada, additional, Topic, Anita, additional, Tomljenovic, Dejan, additional, Greguric, Tomislav, additional, Radovanovic, Patricija Bankovic, additional, Jund, Rainer, additional, Haimerl, Pascal, additional, Chaker, Adam M., additional, Schober, Yvonne, additional, Schindela, Sonja, additional, Nockher, Andreas, additional, Schmidt-Weber, Carsten B., additional, Bieren, Julia Esser-Von, additional, Ickrath, Pascal, additional, Kleinsasser, Norbert, additional, Beyersdorf, Niklas, additional, Ding, Xin, additional, Hagen, Rudolf, additional, Hackenberg, Stephan, additional, Cangiano, Daniela, additional, Cinetto, Francesco, additional, Brescia, Giuseppe, additional, Marioni, Gino, additional, Zanotti, Claudia, additional, Schiavon, Franco, additional, Padoan, Roberto, additional, Caputo, Ilaria, additional, Neri, Raffaella, additional, Agostini, Carlo, additional, Kim, Ji Heui, additional, Jang, Yong Ju, additional, Lim, Ji Youn, additional, Kim, Sung Hee, additional, Savlevich, Elena, additional, Gaganov, Leonid, additional, Kochnova, Maria, additional, Egorov, Victor, additional, Fok, Jie Shen, additional, Hanif, Tanzeela, additional, Renkonen, Jutta, additional, Joenväärä, Sakari, additional, Kankainen, Matti, additional, Mäkelä, Mika, additional, Kauppi, Paula, additional, Pelkonen, Anna, additional, Mattila, Pirkko, additional, Renkonen, Risto, additional, Toppila-Salmi, Sanna, additional, Holtappels, Gabriele, additional, Lambrecht, Bart N., additional, Blanca-López, Natalia, additional, Gonzalez-Visiedo, Miguel, additional, Jurado, Raquel, additional, and Canto, Gabriela, additional

Published
2017
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10. House dust mite drives proinflammatory eicosanoid reprogramming and macrophage effector functions.

Author

Henkel, Fiona D. R., Friedl, Antonie, Haid, Mark, Thomas, Dominique, Bouchery, Tiffany, Haimerl, Pascal, Reyes Jiménez, Marta, Alessandrini, Francesca, Schmidt‐Weber, Carsten B., Harris, Nicola L., Adamski, Jerzy, and Esser‐von Bieren, Julia

Subjects
HOUSE dust mites, NEMATODE infections, HELMINTHIASIS, IMMUNE response, LIPID metabolism
Abstract

Background: Eicosanoid lipid mediators play key roles in type 2 immune responses, for example in allergy and asthma. Macrophages represent major producers of eicosanoids and they are key effector cells of type 2 immunity. We aimed to comprehensively track eicosanoid profiles during type 2 immune responses to house dust mite (HDM) or helminth infection and to identify mechanisms and functions of eicosanoid reprogramming in human macrophages. Methods: We established an LC‐MS/MS workflow for the quantification of 52 oxylipins to analyze mediator profiles in human monocyte‐derived macrophages (MDM) stimulated with HDM and during allergic airway inflammation (AAI) or nematode infection in mice. Expression of eicosanoid enzymes was studied by qPCR and western blot and cytokine production was assessed by multiplex assays. Results: Short (24 h) exposure of alveolar‐like MDM (aMDM) to HDM suppressed 5‐LOX expression and product formation, while triggering prostanoid (thromboxane and prostaglandin D2 and E2) production. This eicosanoid reprogramming was p38‐dependent, but dectin‐2‐independent. HDM also induced proinflammatory cytokine production, but reduced granulocyte recruitment by aMDM. In contrast, high levels of cysteinyl leukotrienes (cysLTs) and 12‐/15‐LOX metabolites were produced in the airways during AAI or nematode infection in mice. Conclusion: Our findings show that a short exposure to allergens as well as ongoing type 2 immune responses are characterized by a fundamental reprogramming of the lipid mediator metabolism with macrophages representing particularly plastic responder cells. Targeting mediator reprogramming in airway macrophages may represent a viable approach to prevent pathogenic lipid mediator profiles in allergy or asthma. [ABSTRACT FROM AUTHOR]

Published
2019
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