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Open AccessArticle

Staphylococcus aureus Lung Infection Results in Down-Regulation of Surfactant Protein-A Mainly Caused by Pro-Inflammatory Macrophages

1
Institute of Medical Microbiology, Jena University Hospital, Am Klinikum1, D-07747 Jena, Germany
2
Section of Experimental Virology, Institute of Medical Microbiology, Jena University Hospital, Hans-Knöll-Str. 2, D-07745 Jena, Germany
3
Applied Systems Biology, Leibniz Institute for Natural Product Research and Infection Biology—Hans Knöll Institute, Adolf-Reichwein-Straße 23, 07745 Jena, Germany
4
Dynamic42, GmbH, Winzerlaer Str. 2, D-07745 Jena, Germany
5
Center for Electron Microscopy, Jena University Hospital, D-07743 Jena, Germany
6
Institute of Biochemistry, Jena University Hospital, D-07743 Jena, Germany
7
Faculty of Biological Sciences, Friedrich Schiller University of Jena, D-07745 Jena, Germany
8
Institute of Microbiology, Faculty of Biological Sciences, Friedrich Schiller University Jena, 07743 Jena, Germany
*
Author to whom correspondence should be addressed.
Microorganisms 2020, 8(4), 577; https://doi.org/10.3390/microorganisms8040577
Received: 16 March 2020 / Revised: 7 April 2020 / Accepted: 14 April 2020 / Published: 16 April 2020
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 Staphylococcus aureus (S. aureus) 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 S. aureus 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 S. aureus. 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 S. aureus 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. View Full-Text
Keywords: Staphylococcus aureus; pneumonia; surfactant protein-A; influenza A virus; human alveolus-on-a-chip Staphylococcus aureus; pneumonia; surfactant protein-A; influenza A virus; human alveolus-on-a-chip
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Schicke, E.; Cseresnyés, Z.; Rennert, K.; Vau, V.; Haupt, K.F.; Hornung, F.; Nietzsche, S.; Swiczak, F.; Schmidtke, M.; Glück, B.; Koch, M.; Schacke, M.; Heller, R.; Mosig, A.S.; Figge, M.T.; Ehrhardt, C.; Löffler, B.; Deinhardt-Emmer, S. Staphylococcus aureus Lung Infection Results in Down-Regulation of Surfactant Protein-A Mainly Caused by Pro-Inflammatory Macrophages. Microorganisms 2020, 8, 577.

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