uu.seUppsala University Publications
Change search
Link to record
Permanent link

Direct link
BETA
Wallenquist, Ulrika
Publications (8 of 8) Show all publications
Wicher, G. K., Wallenquist, U., Lei, Y., Enoksson, M., Li, X., Fuchs, B., . . . Forsberg Nilsson, K. (2017). Interleukin-33 Promotes Recruitment of Microglia/Macrophages in Response to Traumatic Brain Injury. Journal of Neurotrauma, 34(22), 3173-3182
Open this publication in new window or tab >>Interleukin-33 Promotes Recruitment of Microglia/Macrophages in Response to Traumatic Brain Injury
Show others...
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.

Keywords
alarmin, glia, microglia, traumatic brain injury, neuroinflammation
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-341988 (URN)10.1089/neu.2016.4900 (DOI)000414560000013 ()28490277 (PubMedID)
Funder
Swedish Research Council
Available from: 2018-02-16 Created: 2018-02-16 Last updated: 2018-07-13Bibliographically approved
Frick, A., Åhs, F., Michelgård Palmquist, Å., Pissiota, A., Wallenquist, U., Fernandez, M., . . . Fredrikson, M. (2016). Overlapping expression of serotonin transporters and neurokinin-1 receptors in posttraumatic stress disorder: a multi-tracer PET study. Molecular Psychiatry, 21(10), 1400-1407
Open this publication in new window or tab >>Overlapping expression of serotonin transporters and neurokinin-1 receptors in posttraumatic stress disorder: a multi-tracer PET study
Show others...
2016 (English)In: Molecular Psychiatry, ISSN 1359-4184, E-ISSN 1476-5578, Vol. 21, no 10, p. 1400-1407Article in journal (Refereed) Published
Abstract [en]

The brain serotonergic system is colocalized and interacts with the neuropeptidergic substance P/neurokinin-1 (SP/NK1) system. Both these neurochemical systems have independently been implicated in stress and anxiety, but interactions between them might be crucial for human anxiety conditions. Here, we examined the serotonin and substance P/neurokinin-1 (SP/NK1) systems individually as well as their overlapping expression in 16 patients with posttraumatic stress disorder (PTSD) and 16 healthy controls. Participants were imaged with the highly selective radiotracers [(11)C]-3-amino-4-(2-dimethylaminomethylphenylsulfanyl)-benzonitrile (DASB) and [(11)C]GR205171 assessing serotonin transporter (SERT) and NK1 receptor availability, respectively. Voxel-wise analyses in the amygdala, our a priori-defined region of interest, revealed increased number of NK1 receptors, but not SERT in the PTSD group. Symptom severity, as indexed by the Clinician-administered PTSD Scale, was negatively related to SERT availability in the amygdala, and NK1 receptor levels moderated this relationship. Exploratory, voxel-wise whole-brain analyses revealed increased SERT availability in the precentral gyrus and posterior cingulate cortex of PTSD patients. Patients, relative to controls, displayed lower degree of overlapping expression between SERT and NK1 receptors in the putamen, thalamus, insula and lateral orbitofrontal gyrus, lower overlap being associated with higher PTSD symptom severity. Expression overlap also explained more of the symptomatology than did either system individually, underscoring the importance of taking interactions between the neurochemical systems into account. Thus, our results suggest that aberrant serotonergic-SP/NK1 couplings contribute to the pathophysiology of PTSD and, consequently, that normalization of these couplings may be therapeutically important.

National Category
Psychology
Identifiers
urn:nbn:se:uu:diva-268105 (URN)10.1038/mp.2015.180 (DOI)000384127000011 ()26619809 (PubMedID)
Funder
Swedish Research CouncilThe Swedish Brain FoundationRiksbankens JubileumsfondForte, Swedish Research Council for Health, Working Life and Welfare
Available from: 2015-12-02 Created: 2015-12-02 Last updated: 2017-12-01Bibliographically approved
Engman, J., Frick, A., Alaie, I., Björkstrand, J., Ågren, T., Faria, V., . . . Furmark, T. (2013). Altered Amygdala but not Default Mode Network Functional Connectivity in Social Anxiety Disorder. Paper presented at 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry, MAY 16-18, 2013, San Francisco, CA. Biological Psychiatry, 73(9), 79S-79S
Open this publication in new window or tab >>Altered Amygdala but not Default Mode Network Functional Connectivity in Social Anxiety Disorder
Show others...
2013 (English)In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 73, no 9, p. 79S-79SArticle in journal, Meeting abstract (Other academic) Published
Keywords
resting state, functional connectivity, social anxiety disorder, default mode network, amygdala
National Category
Medical and Health Sciences Social Sciences
Identifiers
urn:nbn:se:uu:diva-202475 (URN)000318671800244 ()
Conference
68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry, MAY 16-18, 2013, San Francisco, CA
Available from: 2013-07-01 Created: 2013-06-24 Last updated: 2017-12-06
Frick, A., Engman, J., Alaie, I., Björkstrand, J., Faria, V., Gingnell, M., . . . Furmark, T. (2013). Regional Gray Matter Volume of the Lingual Gyrus is Related to Symptom Severity in Patients with Social Anxiety Disorder. Paper presented at 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry, MAY 16-18, 2013, San Francisco, CA. Biological Psychiatry, 73(9), 79S-80S
Open this publication in new window or tab >>Regional Gray Matter Volume of the Lingual Gyrus is Related to Symptom Severity in Patients with Social Anxiety Disorder
Show others...
2013 (English)In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 73, no 9, p. 79S-80SArticle in journal, Meeting abstract (Other academic) Published
Keywords
social anxiety disorder, social phobia, voxel-based morphometry, structural, imaging
National Category
Medical and Health Sciences Social Sciences
Identifiers
urn:nbn:se:uu:diva-202476 (URN)000318671800245 ()
Conference
68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry, MAY 16-18, 2013, San Francisco, CA
Available from: 2013-07-01 Created: 2013-06-24 Last updated: 2017-12-06Bibliographically approved
Alaie, I., Frick, A., Engman, J., Björkstrand, J., Faria, V., Gingnell, M., . . . Furmark, T. (2013). Symptom Improvement in Social Anxiety Disorder is Associated with Reduced Amygdala Reactivity to Emotional Faces. Paper presented at 68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry, MAY 16-18, 2013, San Francisco, CA. Biological Psychiatry, 73(9), 79S-79S
Open this publication in new window or tab >>Symptom Improvement in Social Anxiety Disorder is Associated with Reduced Amygdala Reactivity to Emotional Faces
Show others...
2013 (English)In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 73, no 9, p. 79S-79SArticle in journal, Meeting abstract (Other academic) Published
Keywords
social anxiety disorder, functional neuroimaging, amygdala reactivity, therapeutic response, emotional face perception
National Category
Medical and Health Sciences Social Sciences
Identifiers
urn:nbn:se:uu:diva-202474 (URN)000318671800243 ()
Conference
68th Annual Scientific Meeting of the Society-of-Biological-Psychiatry, MAY 16-18, 2013, San Francisco, CA
Available from: 2013-07-01 Created: 2013-06-24 Last updated: 2017-12-06Bibliographically approved
Wallenquist, U., Holmqvist, K., Hånell, A., Marklund, N., Hillered, L. & Forsberg-Nilsson, K. (2012). Ibuprofen attenuates the inflammatory response and allows formation of migratory neuroblasts from grafted stem cells after traumatic brain injury. Restorative Neurology and Neuroscience, 30(1), 9-19
Open this publication in new window or tab >>Ibuprofen attenuates the inflammatory response and allows formation of migratory neuroblasts from grafted stem cells after traumatic brain injury
Show others...
2012 (English)In: Restorative Neurology and Neuroscience, ISSN 0922-6028, E-ISSN 1878-3627, Vol. 30, no 1, p. 9-19Article in journal (Refereed) Published
Abstract [en]

Purpose: There is hope for neural stem and progenitor cells (NSPC) to enhance regeneration when transplanted to the injured brain after traumatic brain injury (TBI). So far, the therapeutic effects of NSPC transplantation have been hampered mainly by the notable death of the transplanted cells. Neuroinflammation may lead to additional cell death after TBI and we hypothesized that survival of grafted NSPC could be enhanced by anti-inflammatory treatment.

Methods: Mice that were subjected to controlled cortical impact TBI and grafted with NSPC, were treated with the non-steroidal anti-inflammatory drug ibuprofen.

Results: Ibuprofen was found to down-regulate the TBI-induced inflammatory response. In addition, migrating neuroblasts from transplanted cells were observed near the contusion and in the ipsilateral hippocampus in ibuprofen-treated animals only, suggesting that the anti-inflammatory treatment had beneficial effects on graft survival and/or differentiation. However, Morris Water Maze performance or TBI-induced tissue loss was not influenced by ibuprofen treatment.

Conclusions: Our data suggests that anti-inflammatory strategies may be a complement to enhance the outcome for the cell transplants following TBI.

Keywords
Neural stem cell, regeneration, transplantation, controlled cortical impact, eGFP
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-110094 (URN)10.3233/RNN-2011-0606 (DOI)000300955300002 ()
Available from: 2009-11-03 Created: 2009-11-03 Last updated: 2017-12-12Bibliographically approved
Engman, J., Frick, A., Wallenquist, U., Faria, V., Ågren, T., Larsson, E.-M., . . . Furmark, T. (2012). Neural processing of emotionalfaces in social anxiety disorder. Paper presented at 18th Annual Meeting of the Organization for Human Brain Mapping, Beijing, China.
Open this publication in new window or tab >>Neural processing of emotionalfaces in social anxiety disorder
Show others...
2012 (English)Conference paper, Poster (with or without abstract) (Refereed)
National Category
Psychology
Identifiers
urn:nbn:se:uu:diva-184525 (URN)
Conference
18th Annual Meeting of the Organization for Human Brain Mapping, Beijing, China
Available from: 2012-11-08 Created: 2012-11-08 Last updated: 2012-12-20Bibliographically approved
Brännvall, K., Sandelin, M., Wallenquist, U., Forsberg-Nilsson, K., Aldskogius, H. & Kozlova, E. N. (2006). Central nervous system stem/progenitor cells form neurons and peripheral glia after transplantation to the dorsal root ganglion.. NeuroReport, 17(6), 623-628
Open this publication in new window or tab >>Central nervous system stem/progenitor cells form neurons and peripheral glia after transplantation to the dorsal root ganglion.
Show others...
2006 (English)In: NeuroReport, ISSN 0959-4965, E-ISSN 1473-558X, Vol. 17, no 6, p. 623-628Article in journal (Refereed) Published
Abstract [en]

We asked whether neural stem/progenitor cells from the cerebral cortex of E14.5 enhanced green fluorescent protein transgenic mice are able to survive grafting and differentiate in the adult rat dorsal root ganglion. Neurospheres were placed in lumbar dorsal root ganglion cavities after removal of the dorsal root ganglia. Alternatively, dissociated neurospheres were injected into intact dorsal root ganglia. Enhanced green fluorescent protein-positive cells in the dorsal root ganglion cavity were located in clusters and expressed beta-III-tubulin or glial fibrillary acidic protein after 1 month, whereas after 3 months, surviving grafted cells expressed only glial fibrillary acidic protein. In the intact adult DRG, transplanted neural stem/progenitor cells surrounded dorsal root ganglion cells and fibers, and expressed glial but not neuronal markers. These findings show that central nervous system stem/progenitor cells can survive and differentiate into neurons and peripheral glia after xenotransplantation to the adult dorsal root ganglion.

Keywords
Actins/genetics, animals, cell differentiation/physiology, cells, cultured, Cerebral Cortex/*cytology/embryology, embryo, ganglia, spinal/*cytology/transplantation, gene expression/physiology, green fluorescent, Proteins/genetics, immunohistochemistry/methods, intermediate filament proteins/metabolism, mice, mice, inbred C57BL, transgenic, nerve tissue proteins/metabolism, neuroglia/*physiology, neurons/*physiology, stem cell transplantation/methods, stem cells/*physiology, time factors, tubulin/metabolism, nerve regeneration, neural stem/progenitor cell, satellite cell, Schwann cell, sensory neuron, spinal cord
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-22831 (URN)000237529300013 ()16603923 (PubMedID)
Available from: 2007-03-01 Created: 2007-03-01 Last updated: 2017-12-07Bibliographically approved
Organisations

Search in DiVA

Show all publications