Why and how enteropathogenic E.coli (EPEC) inhibit innate immune response pathways of enterocytes
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1
Newcastle University, Institute for Cell and Molecular Biosciences, United Kingdom
Enteropathogenic E.coli (EPEC) infection of the infant small intestine is annually linked to millions of diarrhoeal cases with up to a 40% mortality rate in some developing countries. Critical to the disease process is a Type Three Secretion System (T3SS) that delivers ‘effector’ proteins into intestinal cells. Prototypic EPEC (E2348/69) has 20 effector-encoding genes of which 6 are co-inherited with the T3SS genes on the Locus of Enterocyte Effacement (LEE) pathogenicity island. Here, I will discuss how we became interested in how EPEC inhibits innate immune responses and describe studies with a disease-relevant small intestinal model that provided a rationale for EPEC to possess an inhibitory mechanism. I will also discuss the linkage of EPEC’s ability to inhibit immune responses to a plausible explanation for the paradoxically-weak inflammation of the disease caused by this barrier- disrupting pathogen and how it predicted inhibitory roles for non-LEE-encoded (Nle) effector(s). Finally, I will review the recent explosion of Nle effector functions implicated in inhibiting immune responses with a more recent, unexpected, finding having implications on the evolution of effector properties and EPEC’s ability to inhibit innate immune responses of infected cells.
Keywords:
EPEC,
Infant,
Nle effector,
T3SS
Conference:
ECMIS - E. coli and the Mucosal Immune System : Interaction, Modulation and Vaccination, Ghent, Belgium, 2 Jul - 5 Jul, 2011.
Presentation Type:
Oral Presentation
Topic:
Infection and innate immunity, immunosupression and/or immunostimulation
Citation:
Kenny
B
(2011). Why and how enteropathogenic E.coli (EPEC) inhibit innate immune response pathways of enterocytes.
Front. Immunol.
Conference Abstract:
ECMIS - E. coli and the Mucosal Immune System : Interaction, Modulation and Vaccination.
doi: 10.3389/conf.fimmu.2011.01.00016
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Received:
22 Sep 2011;
Published Online:
03 Oct 2011.
*
Correspondence:
Prof. Brendan Kenny, Newcastle University, Institute for Cell and Molecular Biosciences, Newcastle, United Kingdom, brendan.kenny@ncl.ac.uk