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Interleukin-33 Promotes Recruitment of Microglia/Macrophages in Response to Traumatic Brain Injury
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Neuro-Oncology. Uppsala University, Science for Life Laboratory, SciLifeLab.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology. Uppsala University, Science for Life Laboratory, SciLifeLab.
Karolinska Inst, Immunol & Allergy Unit, Dept Med, Stockholm, Sweden.;Karolinska Univ Hosp, Stockholm, Sweden..
Karolinska Inst, Immunol & Allergy Unit, Dept Med, Stockholm, Sweden.;Karolinska Univ Hosp, Stockholm, Sweden..
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2017 (English)In: Journal of Neurotrauma, ISSN 0897-7151, E-ISSN 1557-9042, Vol. 34, no 22, p. 3173-3182Article in journal (Refereed) Published
Abstract [en]

Traumatic brain injury (TBI) is a devastating condition, often leading to life-long consequences for patients. Even though modern neurointensive care has improved functional and cognitive outcomes, efficient pharmacological therapies are still lacking. Targeting peripherally derived, or resident inflammatory, cells that are rapid responders to brain injury is promising, but complex, given that the contribution of inflammation to exacerbation versus improved recovery varies with time post-injury. The injury-induced inflammatory response is triggered by release of alarmins, and in the present study we asked whether interleukin-33 (IL-33), an injury-associated nuclear alarmin, is involved in TBI. Here, we used samples from human TBI microdialysate, tissue sections from human TBI, and mouse models of central nervous system injury and found that expression of IL-33 in the brain was elevated from nondetectable levels, reaching a maximum after 72 h in both human samples and mouse models. Astrocytes and oligodendrocytes were the main producers of IL-33. Post-TBI, brains of mice deficient in the IL-33 receptor, ST2, contained fewer microglia/macrophages in the injured region than wild-type mice and had an altered cytokine/chemokine profile in response to injury. These observations indicate that IL-33 plays a role in neuroinflammation with microglia/macrophages being cellular targets for this interleukin post-TBI.

Place, publisher, year, edition, pages
2017. Vol. 34, no 22, p. 3173-3182
Keywords [en]
alarmin, glia, microglia, traumatic brain injury, neuroinflammation
National Category
Neurology
Identifiers
URN: urn:nbn:se:uu:diva-341988DOI: 10.1089/neu.2016.4900ISI: 000414560000013PubMedID: 28490277OAI: oai:DiVA.org:uu-341988DiVA, id: diva2:1183408
Funder
Swedish Research CouncilAvailable from: 2018-02-16 Created: 2018-02-16 Last updated: 2018-07-13Bibliographically approved

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Wicher, Grzegorz K.Wallenquist, UlrikaAbu Hamdeh, SamiMarklund, NiklasHillered, LarsForsberg Nilsson, Karin

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Wicher, Grzegorz K.Wallenquist, UlrikaAbu Hamdeh, SamiMarklund, NiklasHillered, LarsNilsson, GunnarForsberg Nilsson, Karin
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Neuro-OncologyScience for Life Laboratory, SciLifeLabDepartment of Immunology, Genetics and PathologyNeurosurgeryHaematology
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