scholarly journals A Role for Macrophage Inflammatory Protein-3α/CC Chemokine Ligand 20 in Immune Priming During T Cell-Mediated Inflammation of the Central Nervous System

2003 ◽  
Vol 170 (12) ◽  
pp. 6298-6306 ◽  
Author(s):  
Rachel E. Kohler ◽  
Adriana C. Caon ◽  
David O. Willenborg ◽  
Ian Clark-Lewis ◽  
Shaun R. McColl
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
T Cell ◽  
Immune Priming ◽  
Cc Chemokine ◽  
Inflammatory Protein ◽  
Chemokine Ligand ◽  
The Central Nervous System ◽  
Macrophage Inflammatory Protein ◽  
Cc Chemokine Ligand 20

scholarly journals IL-9 Promotes Th17 Cell Migration into the Central Nervous System via CC Chemokine Ligand-20 Produced by Astrocytes

2011 ◽  
Vol 186 (7) ◽  
pp. 4415-4421 ◽  
Author(s):  
Yan Zhou ◽  
Yoshifumi Sonobe ◽  
Tomohiko Akahori ◽  
Shijie Jin ◽  
Jun Kawanokuchi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cell Migration ◽  
Th17 Cell ◽  
Cc Chemokine ◽  
Chemokine Ligand ◽  
The Central Nervous System ◽  
Cc Chemokine Ligand 20

scholarly journals Involvement of fractalkine and macrophage inflammatory protein-1 alpha in moderate-severe depression

2004 ◽  
Vol 13 (3) ◽  
pp. 205-207 ◽  
Author(s):  
Rosaria Alba Merendino ◽  
Giuseppe Di Pasquale ◽  
Filippo De Luca ◽  
Laura Di Pasquale ◽  
Edoardo Ferlazzo ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune Therapy ◽  
Severe Depression ◽  
Mononuclear Phagocytes ◽  
Cytokines And Chemokines ◽  
Inflammatory Protein ◽  
Healthy Donors ◽  
The Central Nervous System ◽  
Macrophage Inflammatory Protein

MODERATE-severe depression (MSD) is linked to overexpression of proinflammatory cytokines and chemokines. Fractalkine (FKN) and macrophage inflammatory protein-1 alpha (MIP-1α) are, respectively, members of CX3C and C-C chemokines, and both are involved in recruiting and activating mononuclear phagocytes in the central nervous system. We analysed the presence of FKN and MIP-1α in sera of untreated MSD patients and healthy donors. High FKN levels were observed in all MSD patients as compared with values only detectable in 26% of healthy donors. MIP-1α was measurable in 20% of patients, while no healthy donors showed detectable chemokine levels. In conclusion, we describe a previously unknown involvement of FKN in the pathogenesis of MSD, suggesting that FKN may represent a target for a specific immune therapy of this disease.

CXC-chemokines KC and macrophage inflammatory protein-2 (MIP-2) synergistically induce leukocyte recruitment to the central nervous system in rats

2003 ◽  
Vol 85 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Petra J.G. Zwijnenburg ◽  
Machteld M.J. Polfliet ◽  
Sandrine Florquin ◽  
Timo K. van den Berg ◽  
Christine D. Dijkstra ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Leukocyte Recruitment ◽  
Inflammatory Protein ◽  
The Central Nervous System ◽  
Macrophage Inflammatory Protein

scholarly journals The role of cytokines in the generation of inflammation and tissue damage in experimental gram-positive meningitis.

1990 ◽  
Vol 171 (2) ◽  
pp. 439-448 ◽  
Author(s):  
K Saukkonen ◽  
S Sande ◽  
C Cioffe ◽  
S Wolpe ◽  
B Sherry ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Brain Edema ◽  
Blood Brain Barrier ◽  
Tissue Damage ◽  
Barrier Permeability ◽  
Inflammatory Protein ◽  
Brain Barrier Permeability ◽  
The Central Nervous System ◽  
Macrophage Inflammatory Protein

Cytokines mediate many host responses to bacterial infections. We determined the inflammatory activities of five cytokines in the central nervous system: TNF-alpha, IL-1 alpha, IL-1 beta, macrophage inflammatory protein 1 (MIP-1), and macrophage inflammatory protein 2 (MIP-2). Using a rabbit model of meningeal inflammation, each cytokine (except IL-1 beta) induced enhanced blood brain barrier permeability, leukocytosis in cerebrospinal fluid, and brain edema. Homologous antibodies to each mediator inhibited leukocytosis and brain edema, and moderately decreased blood brain barrier permeability. In rabbits treated with anti-CD-18 antibody to render neutrophils dysfunctional for adhesion, each cytokine studied lost the ability to cause leukocytosis and brain edema. After intracisternal challenge with pneumococci, antibodies to TNF or IL-1 prevented inflammation, while anti-MIP-1 or anti-MIP-2 caused only a 2-h delay in the onset of inflammation. We suggest these cytokines have multiple inflammatory activities in the central nervous system and contribute to tissue damage during pneumococcal meningitis.

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