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1. Obesity increases allergic airway inflammation that can be successfully treated by oral tolerance

Author

Geissler, Nora, primary, Orola, Maria, additional, Alinaghi, Masoumeh, additional, Nardo, Alexander, additional, Stulnig, Thomas M., additional, Séneca, Joana, additional, Schmid, Anna, additional, Korb, Elke, additional, Svoboda, Tatjana, additional, Garner‐Spitzer, Erika, additional, Kundi, Michael, additional, Ehling‐Schulz, Monika, additional, Schabussova, Irma, additional, Inic‐Kanada, Aleksandra, additional, and Wiedermann, Ursula, additional

Published
2023
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2. Obesity increases allergic airway inflammation that can be successfully treated by oral tolerance.

Author

Geissler, Nora, Orola, Maria, Alinaghi, Masoumeh, Nardo, Alexander, Stulnig, Thomas M., Séneca, Joana, Schmid, Anna, Korb, Elke, Svoboda, Tatjana, Garner‐Spitzer, Erika, Kundi, Michael, Ehling‐Schulz, Monika, Schabussova, Irma, Inic‐Kanada, Aleksandra, and Wiedermann, Ursula

Subjects
LEPTIN, OVALBUMINS, TREATMENT effectiveness, OBESITY, GREEN light, NON-communicable diseases, ALVEOLAR macrophages
Abstract

This article explores the potential link between obesity and respiratory allergies. The study conducted on mice found that obesity exacerbates the allergic response, leading to heightened manifestations compared to lean mice. However, the researchers also discovered that oral tolerance induction can effectively attenuate the allergic response and lung inflammation in obese mice. The findings suggest that mucosal allergen-specific immunomodulation may function by reducing specific inflammatory markers and maintaining certain immune cells in the lungs. [Extracted from the article]

Published
2024
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3. The PNPLA3 I148M variant aggravates inflammation through dysfunctional LXR and PPAR gamma signalling in macrophages

Author

Dixon, Emmanuel Dauda, primary, Claudel, Thierry, additional, Genger, Jakob-Wendelin, additional, Zhu, Ci, additional, Paolini, Erika, additional, Nardo, Alexander D, additional, Stadlmayr, Sarah, additional, Mlitz, Veronika, additional, Fuchs, Claudia, additional, Radtke, Christine, additional, Bergthaler, Andreas, additional, Dongiovanni, Paola, additional, Ellmeier, Wilfried, additional, and Trauner, Michael, additional

Published
2023
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4. The PNPLA3 I148M variant initiates metabolic reprogramming in macrophages

Author

Dixon, Emmanuel Dauda, primary, Claudel, Thierry, additional, Genger, Jakob-Wendelin, additional, Zhu, Ci, additional, Stadlmayr, Sarah, additional, Paolini, Erika, additional, Nardo, Alexander D, additional, Mlitz, Veronika, additional, Fuchs, Claudia, additional, Bergthaler, Andreas, additional, Radtke, Christine, additional, Dongiovanni, Paola, additional, Ellmeier, Wilfried, additional, and Trauner, Michael, additional

Published
2023
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11. Impact of osteopontin on the development of non‐alcoholic liver disease and related hepatocellular carcinoma

Author

Nardo, Alexander D., primary, Grün, Nicole G., additional, Zeyda, Maximilian, additional, Dumanic, Monika, additional, Oberhuber, Georg, additional, Rivelles, Elisa, additional, Helbich, Thomas H., additional, Markgraf, Daniel F., additional, Roden, Michael, additional, Claudel, Thierry, additional, Trauner, Michael, additional, and Stulnig, Thomas M., additional

Published
2020
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12. Pathophysiological mechanisms of liver injury in COVID‐19.

Author

Nardo, Alexander D., Schneeweiss‐Gleixner, Mathias, Bakail, May, Dixon, Emmanuel D., Lax, Sigurd F., and Trauner, Michael

Subjects
*COVID-19, *LIVER injuries, *ADULT respiratory distress syndrome, *EPIDEMICS, *PANDEMICS
Abstract

The recent outbreak of coronavirus disease 2019 (COVID‐19), caused by the Severe Acute Respiratory Syndrome Coronavirus‐2 (SARS‐CoV‐2) has resulted in a world‐wide pandemic. Disseminated lung injury with the development of acute respiratory distress syndrome (ARDS) is the main cause of mortality in COVID‐19. Although liver failure does not seem to occur in the absence of pre‐existing liver disease, hepatic involvement in COVID‐19 may correlate with overall disease severity and serve as a prognostic factor for the development of ARDS. The spectrum of liver injury in COVID‐19 may range from direct infection by SARS‐CoV‐2, indirect involvement by systemic inflammation, hypoxic changes, iatrogenic causes such as drugs and ventilation to exacerbation of underlying liver disease. This concise review discusses the potential pathophysiological mechanisms for SARS‐CoV‐2 hepatic tropism as well as acute and possibly long‐term liver injury in COVID‐19. [ABSTRACT FROM AUTHOR]

Published
2021
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