<it>Chlamydophila pneumoniae </it>derived from inclusions late in the infectious cycle induce aponecrosis in human aortic endothelial cells
<p>Abstract</p> <p>Background</p> <p>Atherosclerosis is still the leading cause of death in the western world. Besides known risk factors studies demonstrating <it>Chlamydophila pneumoniae </it>(<it>C. pneumoniae</it>) to be implicated in the pro...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2008-02-01
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| Series: | BMC Microbiology |
| Online Access: | http://www.biomedcentral.com/1471-2180/8/32 |
| _version_ | 1818963351724621824 |
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| author | Groscurth Peter Sundstroem Hanna Latinovic-Golic Sonja Walch Michael Stoeckli Isabelle Marino Joseph Ziegler Urs Dumrese Claudia |
| author_facet | Groscurth Peter Sundstroem Hanna Latinovic-Golic Sonja Walch Michael Stoeckli Isabelle Marino Joseph Ziegler Urs Dumrese Claudia |
| author_sort | Groscurth Peter |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Background</p> <p>Atherosclerosis is still the leading cause of death in the western world. Besides known risk factors studies demonstrating <it>Chlamydophila pneumoniae </it>(<it>C. pneumoniae</it>) to be implicated in the progression of the disease, little is known about <it>C. pneumoniae </it>infection dynamics. We investigated whether <it>C. pneumoniae </it>induce cell death of human aortic endothelial cells, a cell type involved in the initiation of atherosclerosis, and whether chlamydial spots derive from inclusions.</p> <p>Results</p> <p>Lactate dehydrogenase release revealed host cell death to be dependent on the amounts of <it>Chlamydia </it>used for infection. The morphology of lysed human aortic endothelial cells showed DNA strand breaks simultaneously with cell membrane damage exclusively in cells carrying <it>Chlamydia </it>as spots. Further ultrastructural analysis revealed additional organelle dilation, leading to the definition as aponecrotic cell death of endothelial cells. Exclusive staining of the metabolic active pathogens by chlamydial heat shock protein 60 labelling and ceramide incorporation demonstrated that the bacteria responsible for the induction of aponecrosis had resided in former inclusions. Furthermore, a strong pro-inflammatory molecule, high mobility group box protein 1, was shown to be released from aponecrotic host cells.</p> <p>Conclusion</p> <p>From the data it can be concluded that aponecrosis inducing <it>C. pneumoniae </it>stem from inclusions, since metabolically active bacterial spots are strongly associated with aponecrosis late in the infectious cycle in vascular endothelial cells and metabolic activity was exclusively located inside of inclusions in intact cells. Vice versa initial spot-like infection with metabolically inert bacteria does not have an effect on cell death induction. Hence, <it>C. pneumoniae </it>infection can contribute to atherosclerosis by initial endothelial damage.</p> |
| first_indexed | 2024-12-20T12:43:51Z |
| format | Article |
| id | doaj.art-b1084520d34f4ce6a512712ac36e4011 |
| institution | Directory Open Access Journal |
| issn | 1471-2180 |
| language | English |
| last_indexed | 2024-12-20T12:43:51Z |
| publishDate | 2008-02-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Microbiology |
| spelling | doaj.art-b1084520d34f4ce6a512712ac36e40112022-12-21T19:40:22ZengBMCBMC Microbiology1471-21802008-02-01813210.1186/1471-2180-8-32<it>Chlamydophila pneumoniae </it>derived from inclusions late in the infectious cycle induce aponecrosis in human aortic endothelial cellsGroscurth PeterSundstroem HannaLatinovic-Golic SonjaWalch MichaelStoeckli IsabelleMarino JosephZiegler UrsDumrese Claudia<p>Abstract</p> <p>Background</p> <p>Atherosclerosis is still the leading cause of death in the western world. Besides known risk factors studies demonstrating <it>Chlamydophila pneumoniae </it>(<it>C. pneumoniae</it>) to be implicated in the progression of the disease, little is known about <it>C. pneumoniae </it>infection dynamics. We investigated whether <it>C. pneumoniae </it>induce cell death of human aortic endothelial cells, a cell type involved in the initiation of atherosclerosis, and whether chlamydial spots derive from inclusions.</p> <p>Results</p> <p>Lactate dehydrogenase release revealed host cell death to be dependent on the amounts of <it>Chlamydia </it>used for infection. The morphology of lysed human aortic endothelial cells showed DNA strand breaks simultaneously with cell membrane damage exclusively in cells carrying <it>Chlamydia </it>as spots. Further ultrastructural analysis revealed additional organelle dilation, leading to the definition as aponecrotic cell death of endothelial cells. Exclusive staining of the metabolic active pathogens by chlamydial heat shock protein 60 labelling and ceramide incorporation demonstrated that the bacteria responsible for the induction of aponecrosis had resided in former inclusions. Furthermore, a strong pro-inflammatory molecule, high mobility group box protein 1, was shown to be released from aponecrotic host cells.</p> <p>Conclusion</p> <p>From the data it can be concluded that aponecrosis inducing <it>C. pneumoniae </it>stem from inclusions, since metabolically active bacterial spots are strongly associated with aponecrosis late in the infectious cycle in vascular endothelial cells and metabolic activity was exclusively located inside of inclusions in intact cells. Vice versa initial spot-like infection with metabolically inert bacteria does not have an effect on cell death induction. Hence, <it>C. pneumoniae </it>infection can contribute to atherosclerosis by initial endothelial damage.</p>http://www.biomedcentral.com/1471-2180/8/32 |
| spellingShingle | Groscurth Peter Sundstroem Hanna Latinovic-Golic Sonja Walch Michael Stoeckli Isabelle Marino Joseph Ziegler Urs Dumrese Claudia <it>Chlamydophila pneumoniae </it>derived from inclusions late in the infectious cycle induce aponecrosis in human aortic endothelial cells BMC Microbiology |
| title | <it>Chlamydophila pneumoniae </it>derived from inclusions late in the infectious cycle induce aponecrosis in human aortic endothelial cells |
| title_full | <it>Chlamydophila pneumoniae </it>derived from inclusions late in the infectious cycle induce aponecrosis in human aortic endothelial cells |
| title_fullStr | <it>Chlamydophila pneumoniae </it>derived from inclusions late in the infectious cycle induce aponecrosis in human aortic endothelial cells |
| title_full_unstemmed | <it>Chlamydophila pneumoniae </it>derived from inclusions late in the infectious cycle induce aponecrosis in human aortic endothelial cells |
| title_short | <it>Chlamydophila pneumoniae </it>derived from inclusions late in the infectious cycle induce aponecrosis in human aortic endothelial cells |
| title_sort | it chlamydophila pneumoniae it derived from inclusions late in the infectious cycle induce aponecrosis in human aortic endothelial cells |
| url | http://www.biomedcentral.com/1471-2180/8/32 |
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