Chemokines and Chemokine Receptors in the Brain

1999 ◽  
pp. 295-312 ◽  
Author(s):  
Joseph Hesselgesser ◽  
Richard Horuk
Keyword(s):  
Chemokine Receptors ◽  
The Brain

scholarly journals Neurotrophins modulate the expression of chemokine receptors in the brain

2010 ◽  
Vol 17 (1) ◽  
pp. 58-62 ◽  
Author(s):  
Valeriya Avdoshina ◽  
Jody Becker ◽  
Lee A. Campbell ◽  
Maia Parsadanian ◽  
Timothy Mhyre ◽  
...  
Keyword(s):  
Chemokine Receptors ◽  
The Brain

scholarly journals Transcriptomic Analysis of the Effects of Chemokine Receptor CXCR3 Deficiency on Immune Responses in the Mouse Brain during Toxoplasma gondii Infection

2021 ◽  
Vol 9 (11) ◽  
pp. 2340
Author(s):  
Kousuke Umeda ◽  
Youta Goto ◽  
Kenichi Watanabe ◽  
Nanako Ushio ◽  
Ragab M. Fereig ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Mouse Brain ◽  
Chemokine Receptor ◽  
Chemokine Receptors ◽  
Expression Patterns ◽  
Parasite Burden ◽  
Cxc Chemokine ◽  
Immune Related Genes ◽  
The Brain

The obligate intracellular parasite Toxoplasma gondii infects warm-blooded animals, including humans. We previously revealed through a whole-brain transcriptome analysis that infection with T. gondii in mice causes immune response-associated genes to be upregulated, for instance, chemokines and chemokine receptors such as CXC chemokine receptor 3 (CXCR3) and its ligand CXC chemokine ligand 10 (CXCL10). Here, we describe the effect of CXCR3 on responses against T. gondii infection in the mouse brain. In vivo assays using CXCR3-deficient mice showed that the absence of CXCR3 delayed the normal recovery of body weight and increased the brain parasite burden, suggesting that CXCR3 plays a role in the control of pathology in the brain, the site where chronic infection occurs. Therefore, to further analyze the function of CXCR3 in the brain, we profiled the gene expression patterns of primary astrocytes and microglia by RNA sequencing and subsequent analyses. CXCR3 deficiency impaired the normal upregulation of immune-related genes during T. gondii infection, in astrocytes and microglia alike. Collectively, our results suggest that the immune-related genes upregulated by CXCR3 perform a particular role in controlling pathology when the host is chronically infected with T. gondii in the brain.

Chemokines and Chemokine Receptors in the Brain

2009 ◽  
pp. 173-189 ◽  
Author(s):  
Stéphane Mélik Parsadaniantz ◽  
Ghazal Banisadr ◽  
Philippe Sarret ◽  
William Rostène
Keyword(s):  
Chemokine Receptors ◽  
The Brain

scholarly journals Chemokines and chemokine receptors in the brain: implication in neuroendocrine regulation

2007 ◽  
Vol 38 (3) ◽  
pp. 355-363 ◽  
Author(s):  
Céline Callewaere ◽  
Ghazal Banisadr ◽  
William Rostène ◽  
Stéphane Mélik Parsadaniantz
Keyword(s):  
Chemokine Receptors ◽  
Cell Types ◽  
Normal Brain ◽  
Ability To Act ◽  
The Central Nervous System ◽  
Neuronal Functions ◽  
The Brain ◽  
Neuroendocrine Functions

Chemokines are small secreted proteins that chemoattract and activate immune and non-immune cells both in vivo and in vitro. In addition to their well-established role in the immune system, several recent reports have suggested that chemokines and their receptors may also play a role in the central nervous system (CNS). The best known central action is their ability to act as immunoinflammatory mediators. Indeed, these proteins regulate leukocyte infiltration in the brain during inflammatory and infectious diseases. However, we and others recently demonstrated that they are expressed not only in neuroinflammatory conditions, but also constitutively by different cell types including neurons in the normal brain, suggesting that they may act as modulators of neuronal functions. The goal of this review is to highlight the role of chemokines in the control of neuroendocrine functions. First, we will focus on the expression of chemokines and their receptors in the CNS, with the main spotlight on the neuronal expression in the hypothalamo–pituitary system. Secondly, we will discuss the role – we can now suspect – of chemokines and their receptors in the regulation of neuroendocrine functions. In conclusion, we propose that chemokines can be added to the well-described neuroendocrine regulatory mechanisms, providing an additional fine modulatory tuning system in physiological conditions.

scholarly journals MCP-1 and CCR2 Contribute to Non-Lymphocyte-Mediated Brain Disease Induced by Fr98 Polytropic Retrovirus Infection in Mice: Role for Astrocytes in Retroviral Neuropathogenesis

2004 ◽  
Vol 78 (12) ◽  
pp. 6449-6458 ◽  
Author(s):  
Karin E. Peterson ◽  
John S. Errett ◽  
Tao Wei ◽  
Derek E. Dimcheff ◽  
Richard Ransohoff ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Neurological Disease ◽  
Chemokine Receptors ◽  
Disease Process ◽  
Chemotactic Protein ◽  
The Central Nervous System ◽  
Brain Antibody ◽  
The Brain

ABSTRACT Virus infection of the central nervous system (CNS) often results in chemokine upregulation. Although often associated with lymphocyte recruitment, increased chemokine expression is also associated with non-lymphocyte-mediated CNS disease. In these instances, the effect of chemokine upregulation on neurological disease is unclear. In vitro, several chemokines including monocyte chemotactic protein 1 (MCP-1) protect neurons from apoptosis. Therefore, in vivo, chemokine upregulation may be a protective host response to CNS damage. Alternatively, chemokines may contribute to pathogenesis by stimulating intrinsic brain cells or recruiting macrophages to the brain. To investigate these possibilities, we studied a neurovirulent retrovirus, Fr98, that induces severe non-lymphocyte-mediated neurological disease and causes the upregulation of several chemokines that bind to chemokine receptors CCR2 and CCR5. Knockout mice deficient in CCR2 had reduced susceptibility to Fr98 pathogenesis, with significantly fewer mice developing clinical disease than did wild-type controls. In contrast, no reduction in Fr98-induced disease was observed in CCR5 knockout mice. Thus, signaling through CCR2, but not CCR5, plays an important role in Fr98-mediated pathogenesis. Three ligands for CCR2 (MCP-1, MCP-3, and MCP-5) were upregulated during Fr98 infection of the brain. Antibody-blocking experiments demonstrated that MCP-1 was important for retrovirus-induced neurological disease. In situ hybridization analysis revealed that MCP-1 was expressed by glial fibrillary acidic protein-positive astrocytes. Thus, astrocytes, previously not thought to play an effector role in the disease process were found to contribute to pathogenesis through the production of MCP-1. This study also demonstrates that chemokines can mediate pathogenesis in the CNS in the absence of lymphocytic infiltrate and gives credence to the hypothesis that chemokine upregulation is a mechanism by which retroviruses such as human immunodeficiency virus induce neurological damage.

Chemokine receptors in the brain: A developing story

2003 ◽  
Vol 457 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Phuong B. Tran ◽  
Richard J. Miller
Keyword(s):  
Chemokine Receptors ◽  
The Brain

Chemokine receptors in the brain: their role in HIV infection and pathogenesis

AIDS ◽  
2002 ◽  
Vol 16 (13) ◽  
pp. 1709-1730 ◽  
Author(s):  
Julio Martín-García ◽  
Dennis L. Kolson ◽  
Francisco González-Scarano
Keyword(s):  
Hiv Infection ◽  
Chemokine Receptors ◽  
The Brain
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