Search

Your search keyword '"Bechmann I."' showing total 2 results
Start Over Author "Bechmann I." Topic microglia
2 results on '"Bechmann I."'

1. Decreased microglial numbers in Vav1-Cre+:dicer knock-out mice suggest a second source of microglia beyond yolk sac macrophages.

Author

Bechmann, I., Krueger, M., Fehrenbach, M.K., and Tjwa, M.

Subjects
MICROGLIA, LABORATORY mice, YOLK sac, MACROPHAGES, HEMATOPOIESIS, IMMUNOHISTOCHEMISTRY
Abstract

Microglia represent the resident macrophages of the central nervous system (CNS). While it is clear that microglia recruitment is established by differentiation of primitive yolk sac (YS) macrophages and consecutive invasion of the brain, starting around E8 in rodents (Ginhoux et al., 2010), more recent studies suggest that a non-YS contribution to the microglia population should not entirely be dismissed (Swinnen et al., 2013; Xu et al., 2015). Therefore, we used Vav1-Cre + :dicer knock-out mice in order to study the effect of the post-YS hematopoiesis on the definitive microglial population in late prenatal (E16.5, E18.5) and early postnatal brains (P0, P1). Since Vav1 is thereby exclusively expressed in hematopoietic cells starting at E11, the depletion of the micro RNA processing enzyme dicer in Vav1-positive cells allows interfering with post-YS microglia recruitment. Using this approach, analysis of the number of Iba-1 positive microglia revealed a reduction of microglial numbers by 40% in knock-out mice at P1 compared to their individual control littermates. Noteworthy, immunolabeling for Ki-67 and active caspase 3 confirmed that the differences in the microglial numbers are not related to differential rates of proliferation or apoptosis. Therefore, our data demonstrates that interfering with the definitive hematopoiesis highly impacts on the microglial population, implicating an important role of post-YS hematopoiesis on microglial development and recruitment. [ABSTRACT FROM AUTHOR]

Published
2018
Full Text
View/download PDF

2. CD11c-expressing cells reside in the juxtavascular parenchyma and extend processes into the glia limitans of the mouse nervous system

Author

Kerstin Immig, Carolin Prodinger, Jörg Bunse, Ingo Bechmann, Burkhard Becher, Christine Brandt, Frank L. Heppner, Jon D. Laman, Martin Krüger, Melanie Greter, Fridtjof Schiefenhövel, Medical Oncology, Immunology, University of Zurich, and Bechmann, I

Subjects
Pathology, Neuropil, Time Factors, T-Lymphocytes, 2804 Cellular and Molecular Neuroscience, 10263 Institute of Experimental Immunology, Nervous System, Mice, 0302 clinical medicine, Cytotoxic T cell, Glia limitans, Cerebral Cortex, CD11b Antigen, Microglia, biology, Microfilament Proteins, Age Factors, 3. Good health, medicine.anatomical_structure, 2728 Neurology (clinical), Choroid plexus, Neuroglia, Whole-Body Irradiation, medicine.medical_specialty, Green Fluorescent Proteins, Macrophage-1 Antigen, 610 Medicine & health, Bone Marrow Cells, Mice, Transgenic, Receptors, Cell Surface, Major histocompatibility complex, Pathology and Forensic Medicine, 03 medical and health sciences, Cellular and Molecular Neuroscience, Imaging, Three-Dimensional, Organ Culture Techniques, Immune privilege, Microscopy, Electron, Transmission, SDG 3 - Good Health and Well-being, Parenchyma, Glial Fibrillary Acidic Protein, medicine, Animals, Humans, Lectins, C-Type, Calcium-Binding Proteins, CD11c Antigen, 2734 Pathology and Forensic Medicine, Mice, Inbred C57BL, Animals, Newborn, biology.protein, 570 Life sciences, Neurology (clinical), Bone marrow, Cell Adhesion Molecules, 030217 neurology & neurosurgery, 030215 immunology
Abstract

Recent studies demonstrated that primary immune responses can be induced within the brain depending on vessel-associated cells expressing markers of dendritic cells (DC). Using mice transcribing the green fluorescent protein (GFP) under the promoter of the DC marker CD11c, we determined the distribution, phenotype, and source of CD11c+ cells in non-diseased brains. Predilection areas of multiple sclerosis (MS) lesions (periventricular area, adjacent fibre tracts, and optical nerve) were preferentially populated by CD11c+ cells. Most CD11c+ cells were located within the juxtavascular parenchyma rather than the perivascular spaces. Virtually all CD11c+ cells co-expressed ionized calcium-binding adaptor molecule 1 (IBA-1), CD11b, while detectable levels of major histocompatibility complex II (MHC-II) in non-diseased mice was restricted to CD11c+ cells of the choroid plexus. Cellular processes project into the glia limitans which may allow transport and/or presentation of intraparenchymal antigens to extravasated T cells in perivascular spaces. In chimeric mice bearing CD11c-GFP bone marrow, fluorescent cells appeared in the CNS between 8 and 12 weeks after transplantation. In organotypic slice cultures from CD11c-GFP mice, the number of fluorescent cells strongly increased within 72 h. Strikingly, using anti-CD209, an established marker for human DC, a similar population was detected in human brains. Thus, we show for the first time that CD11c+ cells can not only be recruited from the blood into the parenchyma, but also develop from an intraneural precursor in situ. Dysbalance in their recruitment/development may be an initial step in the pathogenesis of chronic (autoimmune) neuroinflammatory diseases such as MS.

Published
2011

Catalog

Books, media, physical & digital resources
See catalog results