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Cited by 361

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

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

Open access
Saukkonen, K, Sande, S, Cioffe, C, Wolpe, S, Sherry, B, Cerami, A, Tuomanen, E·1990·The Journal of experimental medicine

Abstract

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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Crossref · 10.1084/jem.171.2.439

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Metadata

Authors
Saukkonen, K., Sande, S., Cioffe, C., Wolpe, S., Sherry, B., Cerami, A., & Tuomanen, E.
Venue
The Journal of experimental medicine
Published
1990-02-01
Volume
171
Issue
2
Pages
439-448
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2081555919
Cited by
361
References
2
FWCI
24.88
Type
journal article
Language
en
Open access
bronze

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