Lack of a Functioning P2X7 Receptor Leads to Increased Susceptibility to Toxoplasmic Ileitis

Oral infection of C57BL/6J mice with the protozoan parasite Toxoplasma gondii leads to a lethal inflammatory ileitis. Mice lacking the purinergic receptor P2X7R are acutely susceptible to toxoplasmic ileitis, losing significantly more weight than C57BL/6J mice and exhibiting much greater intestinal...

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Bibliographic Details
Published in:PloS one 2015-06, Vol.10 (6), p.e0129048-e0129048
Main Authors: Miller, Catherine M, Zakrzewski, Alana M, Robinson, Dionne P, Fuller, Stephen J, Walker, Robert A, Ikin, Rowan J, Bao, Shisan J, Grigg, Michael E, Wiley, James S, Smith, Nicholas C
Format: Article
Language:English
Subjects:
Animals
Cysts
Cytokines
Cytokines - metabolism
Disease Models, Animal
Disease Progression
Disease Susceptibility
Health aspects
House mouse
Ileitis
Ileitis - genetics
Ileitis - metabolism
Ileitis - parasitology
Ileitis - pathology
Infection
Inflammation
Inflammation Mediators - metabolism
Inflammatory bowel disease
Intermediates
Intestine
Male
MAP Kinase Signaling System
Mice
Mice, Knockout
NF-kappa B - metabolism
NF-κB protein
Oral infection
Parasites
Parasitic diseases
Protozoa
Reactive nitrogen species
Reactive Nitrogen Species - metabolism
Receptors, Purinergic P2X7 - deficiency
Risk factors
Rodents
Toxoplasma
Toxoplasma gondii
Toxoplasmosis, Animal - genetics
Toxoplasmosis, Animal - metabolism
Toxoplasmosis, Animal - parasitology
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Summary:Oral infection of C57BL/6J mice with the protozoan parasite Toxoplasma gondii leads to a lethal inflammatory ileitis. Mice lacking the purinergic receptor P2X7R are acutely susceptible to toxoplasmic ileitis, losing significantly more weight than C57BL/6J mice and exhibiting much greater intestinal inflammatory pathology in response to infection with only 10 cysts of T. gondii. This susceptibility is not dependent on the ability of P2X7R-deficient mice to control the parasite, which they accomplish just as efficiently as C57BL/6J mice. Rather, susceptibility is associated with elevated ileal concentrations of pro-inflammatory cytokines, reactive nitrogen intermediates and altered regulation of elements of NFκB activation in P2X7R-deficient mice. Our data support the thesis that P2X7R, a well-documented activator of pro-inflammatory cytokine production, also plays an important role in the regulation of intestinal inflammation.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0129048