Details

Autor(en) / Beteiligte

• Sinnberg, Tobias
• Lichtensteiger, Christa
• Ali, Omar Hasan
• Pop, Oltin T
• Jochum, Ann-Kristin
• Risch, Lorenz
• Brugger, Silvio D
• Velic, Ana
• Bomze, David
• Kohler, Philipp
• Vernazza, Pietro
• Albrich, Werner C
• Kahlert, Christian R
• Abdou, Marie-Therese
• Wyss, Nina
• Hofmeister, Kathrin
• Niessner, Heike
• Zinner, Carl
• Gilardi, Mara
• Tzankov, Alexandar
• Röcken, Martin
• Dulovic, Alex
• Shambat, Srikanth Mairpady
• Ruetalo, Natalia
• Buehler, Philipp K
• Scheier, Thomas C
• Jochum, Wolfram
• Kern, Lukas
• Henz, Samuel
• Schneider, Tino
• Kuster, Gabriela M
• Lampart, Maurin
• Siegemund, Martin
• Bingisser, Roland
• Schindler, Michael
• Schneiderhan-Marra, Nicole
• Kalbacher, Hubert
• McCoy, Kathy D
• Spengler, Werner
• Brutsche, Martin H
• Maček, Boris
• Twerenbold, Raphael
• Penninger, Josef M
• Matter, Matthias S
• Flatz, Lukas

Titel

Pulmonary Surfactant Proteins Are Inhibited by Immunoglobulin A Autoantibodies in Severe COVID-19

Ist Teil von

• American journal of respiratory and critical care medicine, 2023-01, Vol.207 (1), p.38-49

Ort / Verlag

United States: American Thoracic Society

Erscheinungsjahr

2023

Quelle

MEDLINE

Beschreibungen/Notizen

• Coronavirus disease 2019 (COVID-19) can lead to acute respiratory distress syndrome with fatal outcomes. Evidence suggests that dysregulated immune responses, including autoimmunity, are key pathogenic factors. To assess whether IgA autoantibodies target lung-specific proteins and contribute to disease severity. We collected 147 blood, 9 lung tissue, and 36 BAL fluid samples from three tertiary hospitals in Switzerland and one in Germany. Severe COVID-19 was defined by the need to administer oxygen. We investigated the presence of IgA autoantibodies and their effects on pulmonary surfactant in COVID-19 using the following methods: immunofluorescence on tissue samples, immunoprecipitations followed by mass spectrometry on BAL fluid samples, enzyme-linked immunosorbent assays on blood samples, and surface tension measurements with medical surfactant. IgA autoantibodies targeting pulmonary surfactant proteins B and C were elevated in patients with severe COVID-19 but not in patients with influenza or bacterial pneumonia. Notably, pulmonary surfactant failed to reduce surface tension after incubation with either plasma or purified IgA from patients with severe COVID-19. Our data suggest that patients with severe COVID-19 harbor IgA autoantibodies against pulmonary surfactant proteins B and C and that these autoantibodies block the function of lung surfactant, potentially contributing to alveolar collapse and poor oxygenation.