IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hobden, J. A.
Right arrow Articles by Hazlett, L. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hobden, J. A.
Right arrow Articles by Hazlett, L. D.

 Previous Article  |  Next Article 

Infect. Immun., 07 1997, 2754-2758, Vol 65, No. 7
Copyright © 1997, American Society for Microbiology

Proinflammatory cytokine deficiency and pathogenesis of Pseudomonas aeruginosa keratitis in aged mice

JA Hobden, SA Masinick, RP Barrett and LD Hazlett
Department of Anatomy/Cell Biology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.

Corneal clarity in young adult Swiss (HSD:ICR) mice is restored after Pseudomonas aeruginosa infection. Previous data showed that this response involves a rapid up-regulation of constitutive intercellular cell adhesion molecule-1 (ICAM-1) and migration of inflammatory cells into the cornea. In contrast, in aged mice, there is no up-regulation of corneal ICAM-1, inflammatory cell infiltration into the cornea is delayed, and the cornea perforates. Therefore, the aim of this study was to test whether specific cytokines which up-regulate ICAM-1 expression differ in young and aged mice. Corneas of young (6- to 8- week-old) and aged (1- to 2-year-old) mice were scarified and inoculated with P. aeruginosa. The eyes were graded for pathologic changes (score 0 to +4); at 6, 12, 24, and 48 h postinfection (p.i.), six mice from each age group were sacrificed. Three corneas from each respective group were excised for quantitation of interleukin-1beta (IL- 1beta), tumor necrosis factor alpha, and gamma interferon (IFN-gamma) by enzyme-linked immunosorbent assay. The remaining three corneas from each age group were harvested for quantitation of viable bacteria by direct plate count determination and for infiltrating polymorphonuclear leukocytes (PMNs) by a myeloperoxidase (MPO) assay. Compared to those of young mice, the corneas of infected aged mice had less IL-1beta at 6 h p.i. (P < or = 0.04) and less IFN-gamma at 12 to 48 h p.i. (P < or = 0.05). Also, compared to those of young mice, corneas of aged mice had fewer PMNs (P < or = 0.008) by the MPO assay at 6 h p.i. and more viable bacteria (P < or = 0.01) per cornea by plate count determination at 24 h p.i. These data suggest that the lack of up-regulation of ocular ICAM-1 in aged mice may reflect a reduction in both IL-1beta and IFN-gamma levels in the infected cornea. Consequently, a sufficient number of PMNs and other inflammatory cells fail to rapidly migrate into the infected corneas of aged mice, the bacterial load is initially greater than that in young mice, and the cornea perforates.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 1997 by the American Society for Microbiology. All rights reserved.