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Orientia tsutsugamushi induced endothelial cell activation via the NOD1-IL-32 pathway

Title
Orientia tsutsugamushi induced endothelial cell activation via the NOD1-IL-32 pathway
Authors
Cho K.-A.Jun Y.H.Suh J.W.Kang J.-S.Choi H.J.Woo S.-Y.
Ewha Authors
최희정우소연조경아
SCOPUS Author ID
최희정scopus; 우소연scopus; 조경아scopus
Issue Date
2010
Journal Title
Microbial Pathogenesis
ISSN
0882-4010JCR Link
Citation
vol. 49, no. 3, pp. 95 - 104
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Orientia tsutsugamushi (OT), the causative agent of scrub typhus, is an obligate intracellular bacterium. In order to verify the inflammatory responses involved in the pathogenesis of scrub typhus, we assessed the cytokine profile of the human endothelial cell line, ECV304, after OT infection. We noted that CCL5, CCL17, IL-1α, IL-6, IL-8, IL-10, IL-15, TNF-α and TNF-β were strongly induced in response to OT. Additionally, IL-32, the candidate modulator for the induction of IL-6 and IL-8, was increased significantly with OT infection and these increases coincided with NOD1 pathway activation. Thus, we hypothesized that NOD1 pathway and IL-32 might act on cytokine release in endothelial cells as a modulator of the inflammation caused by OT infection. NOD1 siRNA resulted in a reduction in IL-32 levels, and also reduced IL-1β, IL-6, IL-8, and ICAM-1 expression in OT-infected ECV304 cells. These changes in IL-1β, IL-6, IL-8, and ICAM-1 induced by NOD1 knockdown were reversed as the result of IL-32 treatment. This indicated that OT infection activated the NOD1 pathway followed by IL-32 secretion, thus resulting in the production and expression of IL-1β, IL-6, IL-8, and ICAM-1. Therefore, IL-32 might perform a role upstream of the inflammatory reaction in endothelial cells of OT infection. © 2010 Elsevier Ltd.
DOI
10.1016/j.micpath.2010.05.001
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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