Robert A. Harris

Hanze University of Applied Sciences

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Harald Lund

Karolinska Institutet

Maja Jagodic

Karolinska University Hospital

Xing‐Mei Zhang

Southern Medical University

Ewoud Ewing

Karolinska Institutet

Lara Kular

Karolinska University Hospital

Maria Needhamsen

Karolinska University Hospital

David Gómez-Cabrero

Navarrabiomed

Jinming Han

Capital Medical University

Tomas Olsson

Karolinska Institutet

Keying Zhu

Karolinska Institutet

Cooperative Institutions

Karolinska Institutet

429

Karolinska University Hospital

266

Uppsala University

Science for Life Laboratory

Indiana University – Purdue University Indianapolis

Lund University

Harvard University

Indiana University School of Medicine

Cincinnati Children's Hospital Medical Center

Duke University

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A Two-to-Five Year Follow-Up of a Pediatric Acute-Onset Neuropsychiatric Syndrome Cohort

Child Psychiatry & Human Development (2021)

Caroline Gromark Eva Hesselmark Ida Gebel Djupedal Maria Silverberg AnnaCarin Horne

Abstract Little is known about the long-term prognosis of children with pediatric acute-onset neuropsychiatric syndrome (PANS). Out of the 46 eligible patients from the Karolinska PANS cohort, 34 consented to participate in a follow-up (median 3.3 years). Participants underwent a thorough clinical evaluation and were classified according to their clinical course. Resulting groups were compared on clinical characteristics and laboratory test results. We observed significant reductions in clinician-rated PANS symptom severity and improved general function. Two patients were classified as remitted, 20 as relapsing–remitting, and 12 as having a chronic-static/progressive course. The latter group had an earlier onset, greater impairment and received more pharmacological and psychological treatments. Although remission was rare, the majority of children with PANS were significantly improved over the follow-up period but a non-negligible minority of patients displayed a chronic-static/progressive course and required additional treatments. The proposed definitions of flare and clinical course may be useful in future clinical trials.

PANDAS

10.1007/s10578-021-01135-4

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Citations (27)

Pennsylvania's Family Caregiver Support Program: A Demonstration Project

Sociological Practice (1993)

Elizabeth K. Keech Robert A. Harris John M. Kelley Lori F. Gerring Christopher P. Peters

Caregiver stress

Family Caregivers

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Repurposing of omeprazole for oligodendrocyte differentiation and remyelination

Brain Research (2018)

Keying Zhu Jingxian Sun Kang Zheng Zaofeng Zou Xi Wu

Remyelination

10.1016/j.brainres.2018.12.037

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Citations (15)

Co-infection with Trypanosoma brucei brucei prevents experimental autoimmune encephalomyelitis in DBA/1 mice through induction of suppressor APCs

International Immunology (2005)

Maja Wållberg Robert A. Harris

The immune system has co-evolved with the infectious agents that challenge it, and in response pathogens have developed different mechanisms to subvert host immunity. A wealth of evidence suggests that infections are important components in the development of a functional immune system, and understanding the modulation of the host immune system by pathogens may offer new therapeutic strategies in a non-infectious setting. We investigated how infection with the protozoan parasite Trypanosoma brucei brucei (Tbb) modulates the autoimmune response to recombinant myelin oligodendrocyte glycoprotein (rMOG) in DBA/1 mice. Mice harbouring a Tbb infection did not develop experimental autoimmune encephalomyelitis (EAE) induced by immunization with rMOG in CFA, an animal model for the human autoimmune disease multiple sclerosis. Additionally, mice infected with the parasite at the time of immunization or 1 week later developed less severe EAE than uninfected controls. Protected mice displayed a markedly diminished rMOG-specific proliferation and IFNγ production in lymph node cells and had correspondingly low titres of serum anti-rMOG IgG. Antigen-presenting cells (APCs) from spleens of Tbb-infected mice presented rMOG less efficiently to rMOG-specific T cells in vitro than did splenic APCs from uninfected mice and could also inhibit antigen-specific proliferation in control in vitro cultures. This suppressive effect is at least in part due to increased release of IL-10. Transfer of splenic APCs from Tbb-infected mice into mice immunized with rMOG-CFA 7 days previously abrogated disease significantly. These findings indicate that infections can prevent autoimmunity and that APCs might be used as immunomodulants.

Myelin oligodendrocyte glycoprotein

Encephalomyelitis

10.1093/intimm/dxh253

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Citations (26)

Phenotyping of Macrophages After Radiolabeling and Safety of Intra-arterial Transplantation Assessed by SPECT/CT and MRI

Cell Transplantation (2023)

Ida Friberger Vamsi Gontu Robert A. Harris Thuy Tran Johan Lundberg

Cell therapy is an integral modality of regenerative medicine. Macrophages are known for their sensitivity to activation stimuli and capability to recruit other immune cells to the sites of injury and healing. In addition, the route of administration can impact engraftment and efficacy of cell therapy, and modern neuro-interventional techniques provide the possibility for selective intra-arterial (IA) delivery to the central nervous system (CNS) with very low risk. The effects of radiolabelling and catheter transport on differentially activated macrophages were evaluated. Furthermore, the safety of selective IA administration of these macrophages to the rabbit brain was assessed by single-photon emission computed tomography/computed tomography (SPECT/CT) and ultra-high-field (9.4 T) magnetic resonance imaging (MRI). Cells were successfully labeled with ( 111 In)In-(oxinate) 3 and passed through a microcatheter with preserved phenotype. No cells were retained in the healthy rabbit brain after IA administration, and no adverse events could be observed either 1 h ( n = 6) or 24 h ( n = 2) after cell administration. The procedure affected both lipopolysaccharide/gamma interferon (LPS/IFNγ) activated cells and interleukin 4 (IL4), interleukin 10 (IL10)/transforming growth factor beta 1 (TGFβ1) activated cells to some degree. The LPS/IFNγ activated cells had a significant increase in their phagocytotic function. Overall, the major impact on the cell phenotypes was due to the radiolabeling and not passage through the catheter. Unstimulated cells were substantially affected by both radiolabeling and catheter administration and are hence not suited for this procedure, while both activated macrophages retained their initial phenotypes. In conclusion, activated macrophages are suitable candidates for targeted IA administration without adverse effects on normal, healthy brain parenchyma.

10.1177/09636897231212780

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The effects of low-dose vincristine on megakaryocyte colony-forming cells and megakaryocyte ploidy

British Journal of Haematology (1984)

Robert A. Harris D. G. Penington

The British Journal of Haematology publishes original research papers in clinical, laboratory and experimental haematology. The Journal also features annotations, reviews, short reports, images in haematology and Letters to the Editor.

Thrombocytosis

Megakaryocytopoiesis

10.1111/j.1365-2141.1984.tb08497.x

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An overlooked subset of Cx3cr1wt/wt microglia in the Cx3cr1CreER-Eyfp/wt mouse has a repopulation advantage over Cx3cr1CreER-Eyfp/wt microglia following microglial depletion

Journal of Neuroinflammation (2022)

Kai Zhou Jinming Han Harald Lund Nageswara Rao Boggavarapu Volker M. Lauschke

Fluorescent reporter labeling and promoter-driven Cre-recombinant technologies have facilitated cellular investigations of physiological and pathological processes, including the widespread use of the Cx3cr1CreER-Eyfp/wt mouse strain for studies of microglia.Immunohistochemistry, Flow Cytometry, RNA sequencing and whole-genome sequencing were used to identify the subpopulation of microglia in Cx3cr1CreER-Eyfp/wt mouse brains. Genetically mediated microglia depletion using Cx3cr1CreER-Eyfp/wtRosa26DTA/wt mice and CSF1 receptor inhibitor PLX3397 were used to deplete microglia. Primary microglia proliferation and migration assay were used for in vitro studies.We unexpectedly identified a subpopulation of microglia devoid of genetic modification, exhibiting higher Cx3cr1 and CX3CR1 expression than Cx3cr1CreER-Eyfp/wtCre+Eyfp+ microglia in Cx3cr1CreER-Eyfp/wt mouse brains, thus termed Cx3cr1highCre-Eyfp- microglia. This subpopulation constituted less than 1% of all microglia under homeostatic conditions, but after Cre-driven DTA-mediated microglial depletion, Cx3cr1highCre-Eyfp- microglia escaped depletion and proliferated extensively, eventually occupying one-third of the total microglial pool. We further demonstrated that the Cx3cr1highCre-Eyfp- microglia had lost their genetic heterozygosity and become homozygous for wild-type Cx3cr1. Therefore, Cx3cr1highCre-Eyfp- microglia are Cx3cr1wt/wtCre-Eyfp-. Finally, we demonstrated that CX3CL1-CX3CR1 signaling regulates microglial repopulation both in vivo and in vitro.Our results raise a cautionary note regarding the use of Cx3cr1CreER-Eyfp/wt mouse strains, particularly when interpreting the results of fate mapping, and microglial depletion and repopulation studies.

CX3CR1

Yellow fluorescent protein

10.1186/s12974-022-02381-6

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Regionalized cell and gene signatures govern oesophageal epithelial homeostasis

bioRxiv (Cold Spring Harbor Laboratory) (2024)

David Grommisch Harald Lund Evelien Eenjes Anaïs Julien Christian Göritz

Abstract Regionalized disease prevalence is a common feature of the gastrointestinal tract. Herein, we employed regionally resolved Smart-seq3 single-cell sequencing, generating a comprehensive cell atlas of the adult mouse oesophagus. Characterizing the oesophageal axis, we unveil non-uniform distribution of epithelial basal cells, fibroblasts and immune cells. In addition, we reveal a position-dependent, but cell subpopulation-independent, transcriptional signature, collectively generating a regionalized oesophageal landscape. Combining in vivo models with organoid co-cultures, we demonstrate that proximal and distal basal progenitor cell states are functionally distinct. We find that proximal fibroblasts are more permissive for organoid growth compared to distal fibroblasts and that the immune cell profile is regionalized in two dimensions, where proximal-distal and epithelial-stromal gradients impact epithelial maintenance. Finally, we predict and verify how WNT-, BMP-, IGF-and NRG-signalling are differentially engaged along the oesophageal axis. We establish a cellular and transcriptional framework for understanding oesophageal regionalization, providing a functional basis for epithelial disease susceptibility.

Organoid

Cell type

10.1101/2024.02.21.581361

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Macrophage Polarization: Decisions That Affect Health

Journal of Clinical & Cellular Immunology (2015)

Charles D. Mills Robert A. Harris Klaus Ley

The constructive – repair – activity is commonly called M2 and the destructive – kill – activity of macrophages is called M1 [10,14]. M2and M1-type activities occur throughout the animal kingdom and are normally induced by macrophages sampling their environs for Damageor PathogenAssociated Molecular Patterns (DAMPs and PAMPs) [15]. By sensing whether to exhibit constructive or destructive activities macrophages are uniquely able to protect hosts in ways best suited to correcting varying non-infectious or infectious threats to hosts.

Affect

Macrophage polarization

10.4172/2155-9899.1000364

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Citations (20)

Metabolic Regulation

Elsevier eBooks (2015)

Mulchand S. Patel Robert A. Harris

Gluconeogenesis

Glycogenolysis

Metabolic pathway

Energy homeostasis

Homeostasis

Ketogenesis

10.1016/b978-0-12-394447-4.10034-3

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Citations (4)