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Am J Clin Exp Immunol 2013;2(1):107-116
Original Article
Blockade of IL-1R signaling diminishes Paneth cell depletion and
Toxoplasma gondii induced ileitis in mice
Bérengère Villeret, Léa Brault, Aurélie Couturier-Maillard, Pauline Robinet, Virginie Vasseur, Thomas Secher, Isabelle
Dimier-Poisson, Muazzam Jacobs, Song-Guo Zheng, Valérie F Quesniaux, Bernhard Ryffel
UMR 7355 Université-CNRS INEM, Orléans, France; IIDMM, University of Cape Town, RSA; UMR 0483 Université-INRA
Immunologie Parasi-taire et Vaccinologie, Biothérapies anti-infectieuses, Université François Rabelais, UFR des
Sciences Pharmaceutiques, 31 avenue Monge, 37200 Tours, France; UR 1282 Infectiologie Animale et Santé Publique,
INRA-Centre de Tours, 37380 Nouzilly, France; Division of Rheuma-tology, Department of Medicine, The Keck School of
Medicine, University of Southern California, Los Angeles, California, United States of America. These authors contributed
equally to this work.
Received February 15, 2013; Accepted February 23, 2013; Epub February 27, 2013; Published March 9, 2013
Abstract: Interleukin 1 is a critical inflammatory mediator and involved in host defense to several pathogens. Oral T.
gondii infection causes lethal ileitis in C57BL/6 (BL6) mice and serves to investigate the mechanisms of acute intestinal
inflammation. Here we show that IL-1 is expressed upon oral T. gondii (76K strain) infection in the small intestine and
mediates ileitis as IL-1R1 deficient mice have reduced neutrophil recruitment in the lamina propria, parasite invasion,
inflammatory lesions and enhanced survival as compared to BL6 infected control mice. Protection in the absence of IL-
1R1 signaling was associated with reduced IFN-γ expression and preserved Paneth cells, while these cells were
eliminated in infected BL6 mice. Furthermore, blockade of IL-1 by IL-1β antibody attenuated inflammation in BL6 mice. In
conclusion, IL-1 signaling contributes to the inflammatory response with increase IFN-γ expression and Paneth cell
depletion upon oral T. gondii infection. (AJCEI1302002).
Keywords: Toxoplasma gondii, IL-1R1 receptor signaling, Paneth neutralizing antibody, inflammation, innate immunity
Address correspondence to: Bernhard Ryffel, CNRS UMR 7355 INEM, 3B rue de la Férollerie, 45071 Orléans Cedex 02,
France. Phone: (0) 2 38 25 54 39; Fax: (0) 2 38 25 79 79; E-mail: bryffel@cnrs-orleans.fr.
Original Article
Blockade of IL-1R signaling diminishes Paneth cell depletion and
Toxoplasma gondii induced ileitis in mice
Bérengère Villeret, Léa Brault, Aurélie Couturier-Maillard, Pauline Robinet, Virginie Vasseur, Thomas Secher, Isabelle
Dimier-Poisson, Muazzam Jacobs, Song-Guo Zheng, Valérie F Quesniaux, Bernhard Ryffel
UMR 7355 Université-CNRS INEM, Orléans, France; IIDMM, University of Cape Town, RSA; UMR 0483 Université-INRA
Immunologie Parasi-taire et Vaccinologie, Biothérapies anti-infectieuses, Université François Rabelais, UFR des
Sciences Pharmaceutiques, 31 avenue Monge, 37200 Tours, France; UR 1282 Infectiologie Animale et Santé Publique,
INRA-Centre de Tours, 37380 Nouzilly, France; Division of Rheuma-tology, Department of Medicine, The Keck School of
Medicine, University of Southern California, Los Angeles, California, United States of America. These authors contributed
equally to this work.
Received February 15, 2013; Accepted February 23, 2013; Epub February 27, 2013; Published March 9, 2013
Abstract: Interleukin 1 is a critical inflammatory mediator and involved in host defense to several pathogens. Oral T.
gondii infection causes lethal ileitis in C57BL/6 (BL6) mice and serves to investigate the mechanisms of acute intestinal
inflammation. Here we show that IL-1 is expressed upon oral T. gondii (76K strain) infection in the small intestine and
mediates ileitis as IL-1R1 deficient mice have reduced neutrophil recruitment in the lamina propria, parasite invasion,
inflammatory lesions and enhanced survival as compared to BL6 infected control mice. Protection in the absence of IL-
1R1 signaling was associated with reduced IFN-γ expression and preserved Paneth cells, while these cells were
eliminated in infected BL6 mice. Furthermore, blockade of IL-1 by IL-1β antibody attenuated inflammation in BL6 mice. In
conclusion, IL-1 signaling contributes to the inflammatory response with increase IFN-γ expression and Paneth cell
depletion upon oral T. gondii infection. (AJCEI1302002).
Keywords: Toxoplasma gondii, IL-1R1 receptor signaling, Paneth neutralizing antibody, inflammation, innate immunity
Address correspondence to: Bernhard Ryffel, CNRS UMR 7355 INEM, 3B rue de la Férollerie, 45071 Orléans Cedex 02,
France. Phone: (0) 2 38 25 54 39; Fax: (0) 2 38 25 79 79; E-mail: bryffel@cnrs-orleans.fr.
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