Loading…
Porcine brain microvascular endothelial cell-derived interleukin-8 is first induced and then degraded by Streptococcus suis
Streptococcus suis is a major pathogen of swine, causing mainly meningitis, and it also represents an emerging zoonotic agent. We investigated its ability to induce the release of pro-inflammatory cytokines and chemokines by porcine brain microvascular endothelial cells (PBMEC). We demonstrated that...
Saved in:
Published in: | Microbial pathogenesis 2009-03, Vol.46 (3), p.135-143 |
---|---|
Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Streptococcus suis is a major pathogen of swine, causing mainly meningitis, and it also represents an emerging zoonotic agent. We investigated its ability to induce the release of pro-inflammatory cytokines and chemokines by porcine brain microvascular endothelial cells (PBMEC). We demonstrated that live
S. suis induced a strong release of interleukin (IL)-6 and IL-8 by PBMEC. We showed that the suilysin (hemolysin) was largely responsible for such stimulation, although cell wall components also contribute to cell stimulation but to a considerably lower extent. Interestingly, IL-8 production by PBMEC became undetectable by increasing either the incubation time or bacterial concentration of certain live
S. suis strains. We further demonstrated that this decrease of IL-8 levels was probably linked to the production of a serine protease by
S. suis. Our results suggest that
S. suis can induce an exacerbated release of inflammatory mediators by swine endothelial cells that could cause a massive recruitment of leukocytes and subsequent blood–brain barrier breakdown facilitating the pathogenesis of
S. suis-induced meningitis. In addition,
S. suis could modulate this response by degrading IL-8 which might delay recruitment of
S. suis killer-neutrophils to the site of inflammation, allowing this pathogen to survive upon its arrival to central nervous system. |
---|---|
ISSN: | 0882-4010 1096-1208 |
DOI: | 10.1016/j.micpath.2008.11.004 |