bioRxivImmunology
Multiplex immunohistochemistry differences between Q fever and atherosclerotic abdominal aortic aneurysms indicate immune suppression
K. R. G. Cortenbach, SCAN, A. H. J. Staal, T. Schoffelen, M. A. J. Gorris, L. L. Van der Woude, A. F. M. Jansen, P. Poyck, R. J. Van Suylen, P. C. Wever, C. P. Bleeker-Rovers, M. Srinivas, K. M. Hebeda, M. van Deuren, J. W. Van der Meer, J. M. De Vries, R. R. J. Van Kimmenade
Abstract
BackgroundChronic Q fever is a zoonosis caused by the bacterium Coxiella burnetii which can manifest as infection of an abdominal aortic aneurysm (AAA). Antibiotic therapy often fails, resulting in severe morbidity and high mortality. Whereas previous studies have focused on inflammatory processes in blood, the aim of this study was to investigate local inflammation in aortic tissue. MethodsMultiplex immunohistochemistry was used to investigate local inflammation in Q fever AAAs compared to atherosclerotic AAAs in aorta tissue specimen. Two six-plex panels were used to study both the innate and adaptive immune system. ResultsQ fever AAAs and atherosclerotic AAAs contained similar numbers of CD68+ macrophages and CD3+ T cells. However, in Q fever AAAs the number of CD68+CD206+ M2 macrophages was increased, while expression of GM-CSF was decreased compared to atherosclerotic AAAs. Furthermore, Q fever AAAs showed an increase in both the number of CD8+ cytotoxic T cells and CD3+FoxP3+ regulatory T cells. Lastly, Q fever AAAs did not contain any well-defined granulomas. ConclusionsThese findings demonstrate that despite the presence of pro-inflammatory effector cells, there is an immune suppressive micro environment in Q fever AAA resulting in persistent local infection with C. burnetii.
- organism: human
- assay: imaging
- research focus: host-pathogen & immune response
- approach: experimental assay
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