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Schicke, Elisabeth; Cseresnyés, Zoltán; Rennert, Knut; Vau, Vanessa; Haupt, Karoline Frieda; Hornung, Franziska; Nietzsche, Sandor; Swiczak, Fatina; Schmidtke, Michaela; Glück, Brigitte; Koch, Mirijam; Schacke, Michael; Heller, Regine; Mosig, Alexander S; Figge, Marc Thilo; Ehrhardt, Christina; Löffler, Bettina; Deinhardt-Emmer, Stefanie
Microorganisms, 04/2020, Letnik: 8, Številka: 4Journal Article
Pneumonia is the leading cause of hospitalization worldwide. Besides viruses, bacterial co-infections dramatically exacerbate infection. In general, surfactant protein-A (SP-A) represents a first line of immune defense. In this study, we analyzed whether influenza A virus (IAV) and/or ( ) infections affect SP-A expression. To closely reflect the situation in the lung, we used a human alveolus-on-a-chip model and a murine pneumonia model. Our results show that can reduce extracellular levels of SP-A, most likely attributed to bacterial proteases. Mono-epithelial cell culture experiments reveal that the expression of SP-A is not directly affected by IAV or . Yet, the mRNA expression of SP-A is strongly down-regulated by TNF-α, which is highly produced by professional phagocytes in response to bacterial infection. By using the human alveolus-on-a-chip model, we show that the down-regulation of SP-A is strongly dependent on macrophages. In a murine model of pneumonia, we can confirm that decreases SP-A levels in vivo. These findings indicate that (I) complex interactions of epithelial and immune cells induce down-regulation of SP-A expression and (II) bacterial mono- and super-infections reduce SP-A expression in the lung, which might contribute to a severe outcome of bacterial pneumonia.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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