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Pertussis toxin–induced inflammatory response exacerbates intracerebral haemorrhage and ischaemic stroke in mice

BACKGROUND: Stroke is a devastating disease, including intracerebral haemorrhage (ICH) and ischaemic stroke. Emerging evidences indicate that systemic inflammatory cascades after stroke contribute to brain damage. However, the direct effects and features of systemic inflammation on brain injury, esp...

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Detalles Bibliográficos
Autores principales: Zou, Ming, Feng, Yan, Xiu, Yuwhen, Li, Yan, Zhang, Ying, Fan, Junwan, Li, Haowen, Cao, Jingli, He, Wenyan, Jin, Wei-Na
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BMJ Publishing Group 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8899681/
https://www.ncbi.nlm.nih.gov/pubmed/34341068
http://dx.doi.org/10.1136/svn-2021-000987
Descripción
Sumario:BACKGROUND: Stroke is a devastating disease, including intracerebral haemorrhage (ICH) and ischaemic stroke. Emerging evidences indicate that systemic inflammatory cascades after stroke contribute to brain damage. However, the direct effects and features of systemic inflammation on brain injury, especially comparing between ischaemic and haemorrhagic stroke, are still obscure. METHODS: Pertussis toxin (PT) was used to build a pro-inflammatory milieu after ICH and ischaemic stroke in mouse model. The neurodeficits, stroke lesion, immune response and blood–brain barrier (BBB) destruction were assessed. RESULTS: In ICH mouse model, PT-induced systemic inflammation exacerbated neurological deficits, and enlarged haemorrhage lesion and perihaematomal oedema. We also found promoted leucocyte infiltration and inflammatory cytokine release into the brain after PT treatment. Moreover, the integrity of the BBB was further disrupted after receiving PT. Furthermore, we demonstrated that PT enhanced brain inflammation and aggravated stroke severity in middle cerebral artery occlusion mouse model. CONCLUSIONS: Our results suggest that PT increases inflammatory response that exacerbates brain injury after ICH or ischaemic stroke in mouse model.