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Bacterial meningitis: the role of transforming growth factor-Beta in innate immunity and secondary brain damage


Malipiero, U; Koedel, U; Pfister, W; Fontana, A (2007). Bacterial meningitis: the role of transforming growth factor-Beta in innate immunity and secondary brain damage. Neurodegenerative Diseases, 4(1):43-50.

Abstract

Project 6 of the NCCR 'Neural Plasticity and Repair' focuses on mechanisms of immunity and tissue damage in autoimmune and infectious diseases of the central nervous system (CNS). In one of the subprojects, the influence of transforming growth factor-beta (TGF-beta) on the immune reactivity of the CNS was investigated. In mice with Streptococcus pneumoniae-induced meningitis, a deletion of TGF-beta receptor II on leukocytes is found to enhance recruitment of neutrophils to the site of infection and to promote bacterial clearance. The improved host defense against S. pneumoniae was associated with an almost complete prevention of meningitis-induced vasculitis, a major intracranial complication leading to brain damage. The data show that endogenous TGF-beta suppresses host defense against bacterial infection in the CNS. This contrasts with findings from other body compartments that suggested that TGF-beta is a powerful chemotactic cytokine and increases microbial clearance.

Project 6 of the NCCR 'Neural Plasticity and Repair' focuses on mechanisms of immunity and tissue damage in autoimmune and infectious diseases of the central nervous system (CNS). In one of the subprojects, the influence of transforming growth factor-beta (TGF-beta) on the immune reactivity of the CNS was investigated. In mice with Streptococcus pneumoniae-induced meningitis, a deletion of TGF-beta receptor II on leukocytes is found to enhance recruitment of neutrophils to the site of infection and to promote bacterial clearance. The improved host defense against S. pneumoniae was associated with an almost complete prevention of meningitis-induced vasculitis, a major intracranial complication leading to brain damage. The data show that endogenous TGF-beta suppresses host defense against bacterial infection in the CNS. This contrasts with findings from other body compartments that suggested that TGF-beta is a powerful chemotactic cytokine and increases microbial clearance.

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13 citations in Web of Science®
16 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Immunology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2007
Deposited On:10 Apr 2009 13:18
Last Modified:04 Aug 2016 07:44
Publisher:Karger
ISSN:1660-2854
Publisher DOI:https://doi.org/10.1159/000100358
PubMed ID:17429218
Permanent URL: https://doi.org/10.5167/uzh-16311

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