Lack of a functioning P2X7 receptor leads to increased susceptibility to toxoplasmic ileitis

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.

Kate Miller

Abstract

Background: Oral infection of C57BL/6J mice with the protozoan parasite Toxoplasma gondii leads to a lethal inflammatory ileitis. Principal Findings: 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 suscep-tibility 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 interme-diates and altered regulation of elements of NFκB activation in P2X7R-deficient mice. Conclusions: 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.

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PLoS ONE

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1932-6203

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Public Library of Science

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DOI

10.1371/journal.pone.0129048