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.

scholarly journals Peripheral Taenia infection increases immunoglobulins in the central nervous system.

2020 ◽  
Author(s):  
Sylvia Carina Van Belle ◽  
Anja de Lange ◽  
Hayley Tomes ◽  
Rodney Lucas ◽  
Vinogran Naidoo ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Taenia Crassiceps ◽  
Blood Brain Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability ◽  
The Central Nervous System

Human cysticercosis is a disease caused by larvae of the cestode Taenia solium. It is the most common cause of adult-acquired epilepsy world-wide where it exacts a debilitating toll on the health and well-being of affected communities. It is commonly assumed that the major symptoms associated with cysticercosis are a result of the direct presence of larvae in the brain. As a result, the possible effect of peripherally located larvae on the central nervous system are not well understood. To address this question, we utilised the Taenia crassiceps intra-peritoneal murine model of cysticercosis, where larvae are restricted to the peritoneal cavity. In this model, previous research has observed behavioural changes in rodents but not the development of seizures. Here we used ELISAs, immunoblotting and the Evans Blue test for blood-brain barrier permeability to explore the central effects of peripheral infection of mice with Taenia crassiceps. We identified high levels of parasite-targeting immunoglobulins in the serum of Taenia crassiceps infected mice. We show that the Taenia crassciceps larvae themselves also contain and release host immunoglobulins over time. Additionally, we describe, for the first time, significantly increased levels of IgG within the hippocampi of infected mice, which are accompanied by changes in blood-brain barrier permeability. However, these Taenia crassiceps induced changes were not accompanied by alterations to the levels of proinflammatory, pro-seizure cytokines in the hippocampus. These findings contribute to the understanding of systemic and neuroimmune responses in the Taenia crassiceps model of cysticercosis, with implications for the pathogenesis of human cysticercosis.

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
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