Long-term immune cell profiling in stroke patients with or without infections

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Long-term immune cell profiling in stroke patients with or without infections. / Sørensen, Nina Vindegaard; Hasseldam, Henrik; Johansen, Flemming Fryd; Kristiansen, Uffe; Overgaard, Karsten; Klingenberg Iversen, Helle; Rasmussen, Rune Skovgaard.

In: International Journal of Neuroscience, Vol. 134, No. 2, 2024, p. 197-205.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Sørensen, NV, Hasseldam, H, Johansen, FF, Kristiansen, U, Overgaard, K, Klingenberg Iversen, H & Rasmussen, RS 2024, 'Long-term immune cell profiling in stroke patients with or without infections', International Journal of Neuroscience, vol. 134, no. 2, pp. 197-205. https://doi.org/10.1080/00207454.2022.2098733

APA

Sørensen, N. V., Hasseldam, H., Johansen, F. F., Kristiansen, U., Overgaard, K., Klingenberg Iversen, H., & Rasmussen, R. S. (2024). Long-term immune cell profiling in stroke patients with or without infections. International Journal of Neuroscience, 134(2), 197-205. https://doi.org/10.1080/00207454.2022.2098733

Vancouver

Sørensen NV, Hasseldam H, Johansen FF, Kristiansen U, Overgaard K, Klingenberg Iversen H et al. Long-term immune cell profiling in stroke patients with or without infections. International Journal of Neuroscience. 2024;134(2):197-205. https://doi.org/10.1080/00207454.2022.2098733

Author

Sørensen, Nina Vindegaard ; Hasseldam, Henrik ; Johansen, Flemming Fryd ; Kristiansen, Uffe ; Overgaard, Karsten ; Klingenberg Iversen, Helle ; Rasmussen, Rune Skovgaard. / Long-term immune cell profiling in stroke patients with or without infections. In: International Journal of Neuroscience. 2024 ; Vol. 134, No. 2. pp. 197-205.

Bibtex

@article{d6638202475242fcb19262e8ad1c8cae,
title = "Long-term immune cell profiling in stroke patients with or without infections",
abstract = "Purpose: Infections are frequent complications in acute ischemic stroke and may be caused by an altered immune response influencing brain damage. We compared long-term immune responses in stroke patients with or without infections during the recovery period by performing a long-term profiling of clinically relevant inflammatory parameters from stroke onset until day 49. Materials and methods: Thirty-four stroke patients were retrospectively included and divided into two groups depending on infection status. Group 1 had no infections (N = 17) and group 2 had post-admission infection (N = 17). The patients were evaluated carefully for infections and evolution of the peripheral inflammatory response. Neutrophils, monocytes, lymphocytes, total leukocytes and C-reactive protein were evaluated in relation to the occurrence and development of infections. In both patient groups, an acute boost in neutrophils and monocytes were observed whereas the opposite was true for lymphocytes. Results: In Group 1, neutrophils and monocytes approached normal levels after 20–30 days, but remained elevated in Group 2. We found an increase in neutrophils (p = 0.01) and leukocytes (p < 0.01) as well as C-reactive protein (p < 0.01) among infected patients. Lymphocytes remained depressed in Group 2, while Group 1 slowly approached baseline levels. In both groups, CRP levels initially increased with a slow return to baseline levels. From day 0 to 49 after stroke, uninfected patients generally experienced a decline in leukocytes, neutrophils and monocytes (all p < 0.05), while no similar changes happened among infected patients. Conclusions: Our study provides an overview of general immune cell kinetics after stroke related to infection status. Immune cell numbers were severely disturbed for weeks after the insult, independent of infection status, although infected patients achieved the highest cell counts of neutrophils, leukocytes and for C-reactive protein. The sustained depression of lymphocytes, especially and paradoxically among infected patients, warrants future studies into the mechanisms behind this, with potential for future therapies aimed at restoring normal immunity and thereby improving patient outcome.",
keywords = "leukocytes, macrophages, neutrophil granulocytes, Stroke, T-cells",
author = "S{\o}rensen, {Nina Vindegaard} and Henrik Hasseldam and Johansen, {Flemming Fryd} and Uffe Kristiansen and Karsten Overgaard and {Klingenberg Iversen}, Helle and Rasmussen, {Rune Skovgaard}",
note = "Publisher Copyright: {\textcopyright} 2022 Informa UK Limited, trading as Taylor & Francis Group.",
year = "2024",
doi = "10.1080/00207454.2022.2098733",
language = "English",
volume = "134",
pages = "197--205",
journal = "International Journal of Neuroscience",
issn = "0020-7454",
publisher = "Taylor & Francis",
number = "2",

}

RIS

TY - JOUR

T1 - Long-term immune cell profiling in stroke patients with or without infections

AU - Sørensen, Nina Vindegaard

AU - Hasseldam, Henrik

AU - Johansen, Flemming Fryd

AU - Kristiansen, Uffe

AU - Overgaard, Karsten

AU - Klingenberg Iversen, Helle

AU - Rasmussen, Rune Skovgaard

N1 - Publisher Copyright: © 2022 Informa UK Limited, trading as Taylor & Francis Group.

PY - 2024

Y1 - 2024

N2 - Purpose: Infections are frequent complications in acute ischemic stroke and may be caused by an altered immune response influencing brain damage. We compared long-term immune responses in stroke patients with or without infections during the recovery period by performing a long-term profiling of clinically relevant inflammatory parameters from stroke onset until day 49. Materials and methods: Thirty-four stroke patients were retrospectively included and divided into two groups depending on infection status. Group 1 had no infections (N = 17) and group 2 had post-admission infection (N = 17). The patients were evaluated carefully for infections and evolution of the peripheral inflammatory response. Neutrophils, monocytes, lymphocytes, total leukocytes and C-reactive protein were evaluated in relation to the occurrence and development of infections. In both patient groups, an acute boost in neutrophils and monocytes were observed whereas the opposite was true for lymphocytes. Results: In Group 1, neutrophils and monocytes approached normal levels after 20–30 days, but remained elevated in Group 2. We found an increase in neutrophils (p = 0.01) and leukocytes (p < 0.01) as well as C-reactive protein (p < 0.01) among infected patients. Lymphocytes remained depressed in Group 2, while Group 1 slowly approached baseline levels. In both groups, CRP levels initially increased with a slow return to baseline levels. From day 0 to 49 after stroke, uninfected patients generally experienced a decline in leukocytes, neutrophils and monocytes (all p < 0.05), while no similar changes happened among infected patients. Conclusions: Our study provides an overview of general immune cell kinetics after stroke related to infection status. Immune cell numbers were severely disturbed for weeks after the insult, independent of infection status, although infected patients achieved the highest cell counts of neutrophils, leukocytes and for C-reactive protein. The sustained depression of lymphocytes, especially and paradoxically among infected patients, warrants future studies into the mechanisms behind this, with potential for future therapies aimed at restoring normal immunity and thereby improving patient outcome.

AB - Purpose: Infections are frequent complications in acute ischemic stroke and may be caused by an altered immune response influencing brain damage. We compared long-term immune responses in stroke patients with or without infections during the recovery period by performing a long-term profiling of clinically relevant inflammatory parameters from stroke onset until day 49. Materials and methods: Thirty-four stroke patients were retrospectively included and divided into two groups depending on infection status. Group 1 had no infections (N = 17) and group 2 had post-admission infection (N = 17). The patients were evaluated carefully for infections and evolution of the peripheral inflammatory response. Neutrophils, monocytes, lymphocytes, total leukocytes and C-reactive protein were evaluated in relation to the occurrence and development of infections. In both patient groups, an acute boost in neutrophils and monocytes were observed whereas the opposite was true for lymphocytes. Results: In Group 1, neutrophils and monocytes approached normal levels after 20–30 days, but remained elevated in Group 2. We found an increase in neutrophils (p = 0.01) and leukocytes (p < 0.01) as well as C-reactive protein (p < 0.01) among infected patients. Lymphocytes remained depressed in Group 2, while Group 1 slowly approached baseline levels. In both groups, CRP levels initially increased with a slow return to baseline levels. From day 0 to 49 after stroke, uninfected patients generally experienced a decline in leukocytes, neutrophils and monocytes (all p < 0.05), while no similar changes happened among infected patients. Conclusions: Our study provides an overview of general immune cell kinetics after stroke related to infection status. Immune cell numbers were severely disturbed for weeks after the insult, independent of infection status, although infected patients achieved the highest cell counts of neutrophils, leukocytes and for C-reactive protein. The sustained depression of lymphocytes, especially and paradoxically among infected patients, warrants future studies into the mechanisms behind this, with potential for future therapies aimed at restoring normal immunity and thereby improving patient outcome.

KW - leukocytes

KW - macrophages

KW - neutrophil granulocytes

KW - Stroke

KW - T-cells

U2 - 10.1080/00207454.2022.2098733

DO - 10.1080/00207454.2022.2098733

M3 - Journal article

C2 - 35791087

AN - SCOPUS:85134514139

VL - 134

SP - 197

EP - 205

JO - International Journal of Neuroscience

JF - International Journal of Neuroscience

SN - 0020-7454

IS - 2

ER -

ID: 315252153