Staphylococcus aureus infected embolic stroke upregulates Orm1 and Cxcl2 in a rat model of septic stroke pathology

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Staphylococcus aureus infected embolic stroke upregulates Orm1 and Cxcl2 in a rat model of septic stroke pathology. / Astrup, Lærke Boye; Skovgaard, Kerstin; Rasmussen, Rune Skovgaard; Iburg, Tine Moesgaard; Agerholm, Jørgen Steen; Aalbæk, Bent; Jensen, Henrik Elvang; Nielsen, Ole Lerberg; Johansen, Flemming Fryd; Heegaard, Peter Mikael Helweg; Leifsson, Páll Skúli.

In: Neurological Research, Vol. 41, No. 5, 2019, p. 399-412.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Astrup, LB, Skovgaard, K, Rasmussen, RS, Iburg, TM, Agerholm, JS, Aalbæk, B, Jensen, HE, Nielsen, OL, Johansen, FF, Heegaard, PMH & Leifsson, PS 2019, 'Staphylococcus aureus infected embolic stroke upregulates Orm1 and Cxcl2 in a rat model of septic stroke pathology', Neurological Research, vol. 41, no. 5, pp. 399-412. https://doi.org/10.1080/01616412.2019.1573455

APA

Astrup, L. B., Skovgaard, K., Rasmussen, R. S., Iburg, T. M., Agerholm, J. S., Aalbæk, B., ... Leifsson, P. S. (2019). Staphylococcus aureus infected embolic stroke upregulates Orm1 and Cxcl2 in a rat model of septic stroke pathology. Neurological Research, 41(5), 399-412. https://doi.org/10.1080/01616412.2019.1573455

Vancouver

Astrup LB, Skovgaard K, Rasmussen RS, Iburg TM, Agerholm JS, Aalbæk B et al. Staphylococcus aureus infected embolic stroke upregulates Orm1 and Cxcl2 in a rat model of septic stroke pathology. Neurological Research. 2019;41(5):399-412. https://doi.org/10.1080/01616412.2019.1573455

Author

Astrup, Lærke Boye ; Skovgaard, Kerstin ; Rasmussen, Rune Skovgaard ; Iburg, Tine Moesgaard ; Agerholm, Jørgen Steen ; Aalbæk, Bent ; Jensen, Henrik Elvang ; Nielsen, Ole Lerberg ; Johansen, Flemming Fryd ; Heegaard, Peter Mikael Helweg ; Leifsson, Páll Skúli. / Staphylococcus aureus infected embolic stroke upregulates Orm1 and Cxcl2 in a rat model of septic stroke pathology. In: Neurological Research. 2019 ; Vol. 41, No. 5. pp. 399-412.

Bibtex

@article{d10a9f16029247b1a6804022e11073c6,
title = "Staphylococcus aureus infected embolic stroke upregulates Orm1 and Cxcl2 in a rat model of septic stroke pathology",
abstract = "Objective: Ischaemic brain lesions and brain abscesses are frequent in both human and animal cases of septic embolic stroke. However, existing models of brain infection do not reflect central aspects of septic embolic stroke. Our aim was to compare septic and non-septic embolic stroke in order to identify gene expressions, inflammatory mediators and brain damage in a rat model. Methods: We created precisely located focal brain infarcts in a rat model of Staphylococcus aureus infected embolic stroke. To cause septic embolic stroke we used a fibrin-rich embolus with bacteria, while every rat in the control group received a non-infected embolus. 64 rats were randomized to receive sham-surgery, sterile embolic stroke or septic embolic stroke. All groups were compared for brain pathology, mortality, gene expressions and inflammatory mediators using histology and reverse transcription quantitative real-time PCR. Results: Although infarct volumes did not differ, septic embolic stroke caused higher mortality than sterile embolic stroke (p=  0.002). Brain abscesses were observed only in the septic group. Approximately 400–500 fold increases were observed for Orm1 and Cxcl2 respectively (1.00E-08 < p < 1.92E-07) in the septic group compared to the sterile group, and these were the most dramatically regulated genes in septic embolic stroke compared to sterile embolic stroke. Conclusions: Septic embolic stroke caused brain abscesses, increased mortality and upregulated Orm1 and Cxcl2 gene expressions compared to non-infected embolic stroke. The dramatic Orm1 increase observed in the septic group is unprecedented and suggests a significant biological role of Orm1 during septic neuroinflammation.",
keywords = "abscess, animal model, Embolic stroke, gene expressions, neuroinflammation, septic",
author = "Astrup, {L{\ae}rke Boye} and Kerstin Skovgaard and Rasmussen, {Rune Skovgaard} and Iburg, {Tine Moesgaard} and Agerholm, {J{\o}rgen Steen} and Bent Aalb{\ae}k and Jensen, {Henrik Elvang} and Nielsen, {Ole Lerberg} and Johansen, {Flemming Fryd} and Heegaard, {Peter Mikael Helweg} and Leifsson, {P{\'a}ll Sk{\'u}li}",
year = "2019",
doi = "10.1080/01616412.2019.1573455",
language = "English",
volume = "41",
pages = "399--412",
journal = "Neurological Research",
issn = "0161-6412",
publisher = "Taylor & Francis",
number = "5",

}

RIS

TY - JOUR

T1 - Staphylococcus aureus infected embolic stroke upregulates Orm1 and Cxcl2 in a rat model of septic stroke pathology

AU - Astrup, Lærke Boye

AU - Skovgaard, Kerstin

AU - Rasmussen, Rune Skovgaard

AU - Iburg, Tine Moesgaard

AU - Agerholm, Jørgen Steen

AU - Aalbæk, Bent

AU - Jensen, Henrik Elvang

AU - Nielsen, Ole Lerberg

AU - Johansen, Flemming Fryd

AU - Heegaard, Peter Mikael Helweg

AU - Leifsson, Páll Skúli

PY - 2019

Y1 - 2019

N2 - Objective: Ischaemic brain lesions and brain abscesses are frequent in both human and animal cases of septic embolic stroke. However, existing models of brain infection do not reflect central aspects of septic embolic stroke. Our aim was to compare septic and non-septic embolic stroke in order to identify gene expressions, inflammatory mediators and brain damage in a rat model. Methods: We created precisely located focal brain infarcts in a rat model of Staphylococcus aureus infected embolic stroke. To cause septic embolic stroke we used a fibrin-rich embolus with bacteria, while every rat in the control group received a non-infected embolus. 64 rats were randomized to receive sham-surgery, sterile embolic stroke or septic embolic stroke. All groups were compared for brain pathology, mortality, gene expressions and inflammatory mediators using histology and reverse transcription quantitative real-time PCR. Results: Although infarct volumes did not differ, septic embolic stroke caused higher mortality than sterile embolic stroke (p=  0.002). Brain abscesses were observed only in the septic group. Approximately 400–500 fold increases were observed for Orm1 and Cxcl2 respectively (1.00E-08 < p < 1.92E-07) in the septic group compared to the sterile group, and these were the most dramatically regulated genes in septic embolic stroke compared to sterile embolic stroke. Conclusions: Septic embolic stroke caused brain abscesses, increased mortality and upregulated Orm1 and Cxcl2 gene expressions compared to non-infected embolic stroke. The dramatic Orm1 increase observed in the septic group is unprecedented and suggests a significant biological role of Orm1 during septic neuroinflammation.

AB - Objective: Ischaemic brain lesions and brain abscesses are frequent in both human and animal cases of septic embolic stroke. However, existing models of brain infection do not reflect central aspects of septic embolic stroke. Our aim was to compare septic and non-septic embolic stroke in order to identify gene expressions, inflammatory mediators and brain damage in a rat model. Methods: We created precisely located focal brain infarcts in a rat model of Staphylococcus aureus infected embolic stroke. To cause septic embolic stroke we used a fibrin-rich embolus with bacteria, while every rat in the control group received a non-infected embolus. 64 rats were randomized to receive sham-surgery, sterile embolic stroke or septic embolic stroke. All groups were compared for brain pathology, mortality, gene expressions and inflammatory mediators using histology and reverse transcription quantitative real-time PCR. Results: Although infarct volumes did not differ, septic embolic stroke caused higher mortality than sterile embolic stroke (p=  0.002). Brain abscesses were observed only in the septic group. Approximately 400–500 fold increases were observed for Orm1 and Cxcl2 respectively (1.00E-08 < p < 1.92E-07) in the septic group compared to the sterile group, and these were the most dramatically regulated genes in septic embolic stroke compared to sterile embolic stroke. Conclusions: Septic embolic stroke caused brain abscesses, increased mortality and upregulated Orm1 and Cxcl2 gene expressions compared to non-infected embolic stroke. The dramatic Orm1 increase observed in the septic group is unprecedented and suggests a significant biological role of Orm1 during septic neuroinflammation.

KW - abscess

KW - animal model

KW - Embolic stroke

KW - gene expressions

KW - neuroinflammation

KW - septic

U2 - 10.1080/01616412.2019.1573455

DO - 10.1080/01616412.2019.1573455

M3 - Journal article

VL - 41

SP - 399

EP - 412

JO - Neurological Research

JF - Neurological Research

SN - 0161-6412

IS - 5

ER -

ID: 216929303