Distinct inflammatory responses differentiate cerebral infarct from transient ischaemic attack
We previously reported on a 26-year-old patient who presented early during a large and eventually fatal cerebral infarct. Microarray analysis of blood samples from this patient demonstrated initially up-regulated and subsequently down-regulated Granzyme B (GzmB) expression, along with progressive up...
| Main Authors: | , , , , , |
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| Format: | Journal Article |
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Elsevier
2017
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| Online Access: | http://hdl.handle.net/20.500.11937/69453 |
| _version_ | 1848762044930588672 |
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| author | Armstrong, C. Bosio, E. Neil, C. Brown, S. Hankey, G. Fatovich, Daniel |
| author_facet | Armstrong, C. Bosio, E. Neil, C. Brown, S. Hankey, G. Fatovich, Daniel |
| author_sort | Armstrong, C. |
| building | Curtin Institutional Repository |
| collection | Online Access |
| description | We previously reported on a 26-year-old patient who presented early during a large and eventually fatal cerebral infarct. Microarray analysis of blood samples from this patient demonstrated initially up-regulated and subsequently down-regulated Granzyme B (GzmB) expression, along with progressive up-regulation of genes for S100 calcium binding protein A12 (S100A12) and matrix metalloproteinase 9 (MMP-9). To confirm these findings, we investigated these parameters in patients with suspected stroke presenting within 6 h of symptom onset to a single centre. Blood samples were taken at enrolment, then 1 h, 3 h and 24 h post-enrolment for the examination of cellular, protein and genetic changes. Patients with subsequently confirmed ischaemic (n = 18) or haemorrhagic stroke (n = 11) showed increased intracellular concentrations of GzmB in all cell populations investigated (CD8+, CD8-and Natural Killer [NK] cells). Infarct patients, however, demonstrated significantly reduced GzmB gene expression and increased circulating MMP-9 and S100A12 levels in contrast to transient ischaemic attack (TIA) patients or healthy controls. Furthermore, a pronounced neutrophilia was noted in the infarct and haemorrhage groups, while TIA patients (n = 9) reflected healthy controls (n = 10). These findings suggest a spectrum of immune response during stroke. TIA showed few immunological changes in comparison to infarct and haemorrhage, which demonstrated inhibition of GzmB production and a rise in neutrophil numbers and neutrophil-associated mediators. This implies a greater role of the innate immune system. These markers may provide novel targets for inhibition and reduction of secondary injury. |
| first_indexed | 2025-11-14T10:41:19Z |
| format | Journal Article |
| id | curtin-20.500.11937-69453 |
| institution | Curtin University Malaysia |
| institution_category | Local University |
| last_indexed | 2025-11-14T10:41:19Z |
| publishDate | 2017 |
| publisher | Elsevier |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | curtin-20.500.11937-694532018-10-15T04:36:37Z Distinct inflammatory responses differentiate cerebral infarct from transient ischaemic attack Armstrong, C. Bosio, E. Neil, C. Brown, S. Hankey, G. Fatovich, Daniel We previously reported on a 26-year-old patient who presented early during a large and eventually fatal cerebral infarct. Microarray analysis of blood samples from this patient demonstrated initially up-regulated and subsequently down-regulated Granzyme B (GzmB) expression, along with progressive up-regulation of genes for S100 calcium binding protein A12 (S100A12) and matrix metalloproteinase 9 (MMP-9). To confirm these findings, we investigated these parameters in patients with suspected stroke presenting within 6 h of symptom onset to a single centre. Blood samples were taken at enrolment, then 1 h, 3 h and 24 h post-enrolment for the examination of cellular, protein and genetic changes. Patients with subsequently confirmed ischaemic (n = 18) or haemorrhagic stroke (n = 11) showed increased intracellular concentrations of GzmB in all cell populations investigated (CD8+, CD8-and Natural Killer [NK] cells). Infarct patients, however, demonstrated significantly reduced GzmB gene expression and increased circulating MMP-9 and S100A12 levels in contrast to transient ischaemic attack (TIA) patients or healthy controls. Furthermore, a pronounced neutrophilia was noted in the infarct and haemorrhage groups, while TIA patients (n = 9) reflected healthy controls (n = 10). These findings suggest a spectrum of immune response during stroke. TIA showed few immunological changes in comparison to infarct and haemorrhage, which demonstrated inhibition of GzmB production and a rise in neutrophil numbers and neutrophil-associated mediators. This implies a greater role of the innate immune system. These markers may provide novel targets for inhibition and reduction of secondary injury. 2017 Journal Article http://hdl.handle.net/20.500.11937/69453 10.1016/j.jocn.2016.09.011 Elsevier restricted |
| spellingShingle | Armstrong, C. Bosio, E. Neil, C. Brown, S. Hankey, G. Fatovich, Daniel Distinct inflammatory responses differentiate cerebral infarct from transient ischaemic attack |
| title | Distinct inflammatory responses differentiate cerebral infarct from transient ischaemic attack |
| title_full | Distinct inflammatory responses differentiate cerebral infarct from transient ischaemic attack |
| title_fullStr | Distinct inflammatory responses differentiate cerebral infarct from transient ischaemic attack |
| title_full_unstemmed | Distinct inflammatory responses differentiate cerebral infarct from transient ischaemic attack |
| title_short | Distinct inflammatory responses differentiate cerebral infarct from transient ischaemic attack |
| title_sort | distinct inflammatory responses differentiate cerebral infarct from transient ischaemic attack |
| url | http://hdl.handle.net/20.500.11937/69453 |