Differences in local immune cell landscape between Q fever and atherosclerotic abdominal aortic aneurysms identified by multiplex immunohistochemistry
Chronic Q fever is a zoonosis caused by the bacterium 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 stu...
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Published in | eLife Vol. 11 |
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Main Authors | , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
eLife Sciences Publications Ltd
09.02.2022
eLife Sciences Publications, Ltd |
Subjects | |
Online Access | Get full text |
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Summary: | Chronic Q fever is a zoonosis caused by the bacterium
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.
Multiplex 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 systems.
Q 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
CD8
FoxP3
regulatory T cells. Finally, Q fever AAAs did not contain any well-defined granulomas.
These findings demonstrate that despite the presence of pro-inflammatory effector cells, persistent local infection with
is associated with an immune-suppressed microenvironment.
This work was supported by SCAN consortium: European Research Area - CardioVascualar Diseases (ERA-CVD) grant [JTC2017-044] and TTW-NWO open technology grant [STW-14716]. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. |
ISSN: | 2050-084X 2050-084X |
DOI: | 10.7554/ELIFE.72486 |