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Interleukin-18 gene-deficient mice show enhanced defense and reduced inflammation during pneumococcal meningitis.

Abstract：

:To determine the role of endogenous interleukin-18 (IL-18) in pneumococcal meningitis, meningitis was induced in IL-18 gene-deficient (IL-18(-/-)) and wild-type (WT) mice by intranasal inoculation of Streptococcus pneumoniae with hyaluronidase. Induction of meningitis resulted in an upregulation of both pro- and mature IL-18 in brain tissue in WT mice. IL-18(-/-) and WT mice were equally susceptible to develop meningitis after intranasal infection, yet IL-18(-/-) mice showed a prolonged survival and a suppressed inflammatory response, as reflected by a less profound inflammatory infiltrate around the meninges and lower concentrations of cytokines and chemokines in brain tissue. These findings suggest that endogenous IL-18 contributes to a detrimental inflammatory response during pneumococcal meningitis and that elimination of IL-18 may improve the outcome of this disease.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Zwijnenburg PJ,van der Poll T,Florquin S,Akira S,Takeda K,Roord JJ,van Furth AM

doi

10.1016/s0165-5728(03)00088-2

subject

Has Abstract

pub_date

2003-05-01 00:00:00

pages

31-7

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165572803000882

journal_volume

138

pub_type

杂志文章

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