Vareille, Marjolaine; Rannou, François; Thélier, Natacha; Glasser, Anne-Lise; de Sablet, Thibaut; Martin, Christine; Gobert, Alain P (2008). Heme oxygenase-1 is a critical regulator of nitric oxide production in enterohemorrhagic Escherichia coli-infected human enterocytes. Journal of immunology, 180(8), pp. 5720-6. Bethesda, Md.: American Association of Immunologists
Full text not available from this repository. (Request a copy)Enterohemorrhagic Escherichia coli (EHEC) are the causative agent of hemolytic-uremic syndrome. In the first stage of the infection, EHEC interact with human enterocytes to modulate the innate immune response. Inducible NO synthase (iNOS)-derived NO is a critical mediator of the inflammatory response of the infected intestinal mucosa. We therefore aimed to analyze the role of EHEC on iNOS induction in human epithelial cell lines. In this regard, we show that EHEC down-regulate IFN-gamma-induced iNOS mRNA expression and NO production in Hct-8, Caco-2, and T84 cells. This inhibitory effect occurs through the decrease of STAT-1 activation. In parallel, we demonstrate that EHEC stimulate the rapid inducible expression of the gene hmox-1 that encodes for the enzyme heme oxygenase-1 (HO-1). Knock-down of hmox-1 gene expression by small interfering RNA or the blockade of HO-1 activity by zinc protoporphyrin IX abrogated the EHEC-dependent inhibition of STAT-1 activation and iNOS mRNA expression in activated human enterocytes. These results highlight a new strategy elaborated by EHEC to control the host innate immune response.
Item Type: |
Journal Article (Original Article) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Department of Gynaecology, Paediatrics and Endocrinology (DFKE) > Clinic of Paediatric Medicine |
UniBE Contributor: |
Vareille, Marjolaine |
ISSN: |
0022-1767 |
ISBN: |
18390757 |
Publisher: |
American Association of Immunologists |
Language: |
English |
Submitter: |
Anette van Dorland |
Date Deposited: |
04 Oct 2013 15:03 |
Last Modified: |
05 Dec 2022 14:19 |
PubMed ID: |
18390757 |
Web of Science ID: |
000257506900063 |
URI: |
https://boris.unibe.ch/id/eprint/27251 (FactScience: 105163) |
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