The Experts below are selected from a list of 90 Experts worldwide ranked by ideXlab platform
Marie-denise Linas - One of the best experts on this subject based on the ideXlab platform.
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IL-13 attenuates Gastrointestinal Candidiasis in normal and immunodeficient RAG-2(-/-) mice via peroxisome proliferator-activated receptor-gamma activation.
Journal of Immunology, 2008Co-Authors: Agnès Coste, Céline Lagane, Cédric Filipe, Hélène Authier, Amandine Galès, José Bernad, Victorine Douin-echinard, Jean-claude Lepert, Patricia Balard, Marie-denise LinasAbstract:We recently demonstrated that in vitro peroxisome proliferator-activated receptor-gamma (PPARgamma) activation of mouse peritoneal macrophages by IL-13 or PPARgamma ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2(-/-)) mice with natural and synthetic PPARgamma-specific ligands or with IL-13 decreases C. albicans colonization of the Gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARgamma antagonist, and are reduced in PPARgamma(+/-) mice. Overall, these data demonstrate that IL-13 or PPARgamma ligands attenuate C. albicans infection of the GI tract through PPARgamma activation and hence suggest that PPARgamma ligands may be of therapeutic value in esophageal and GI Candidiasis in immunocompromised patients.
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il 13 attenuates Gastrointestinal Candidiasis in normal and immunodeficient rag 2 mice via peroxisome proliferator activated receptor gamma activation
Journal of Immunology, 2008Co-Authors: Agnès Coste, Céline Lagane, Cédric Filipe, Hélène Authier, Amandine Galès, José Bernad, Jean-claude Lepert, Patricia Balard, Victorine Douinechinard, Marie-denise LinasAbstract:We recently demonstrated that in vitro peroxisome proliferator-activated receptor-gamma (PPARgamma) activation of mouse peritoneal macrophages by IL-13 or PPARgamma ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2(-/-)) mice with natural and synthetic PPARgamma-specific ligands or with IL-13 decreases C. albicans colonization of the Gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARgamma antagonist, and are reduced in PPARgamma(+/-) mice. Overall, these data demonstrate that IL-13 or PPARgamma ligands attenuate C. albicans infection of the GI tract through PPARgamma activation and hence suggest that PPARgamma ligands may be of therapeutic value in esophageal and GI Candidiasis in immunocompromised patients.
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IL-13 Attenuates Gastrointestinal Candidiasis in Normal and Immunodeficient RAG-2−/− Mice via Peroxisome Proliferator-Activated Receptor-γ Activation
Journal of immunology (Baltimore Md. : 1950), 2008Co-Authors: Agnès Coste, Céline Lagane, Cédric Filipe, Hélène Authier, Amandine Galès, José Bernad, Victorine Douin-echinard, Jean-claude Lepert, Patricia Balard, Marie-denise LinasAbstract:We recently demonstrated that in vitro peroxisome proliferator-activated receptor-gamma (PPARgamma) activation of mouse peritoneal macrophages by IL-13 or PPARgamma ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2(-/-)) mice with natural and synthetic PPARgamma-specific ligands or with IL-13 decreases C. albicans colonization of the Gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARgamma antagonist, and are reduced in PPARgamma(+/-) mice. Overall, these data demonstrate that IL-13 or PPARgamma ligands attenuate C. albicans infection of the GI tract through PPARgamma activation and hence suggest that PPARgamma ligands may be of therapeutic value in esophageal and GI Candidiasis in immunocompromised patients.
Agnès Coste - One of the best experts on this subject based on the ideXlab platform.
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oral administration of lactobacillus helveticus la401 and lactobacillus gasseri la806 combination attenuates oesophageal and Gastrointestinal Candidiasis and consequent gut inflammation in mice
Journal of Fungi, 2021Co-Authors: Hélène Authier, Marie Salon, Mouna Rahabi, Benedicte Bertrand, Claude Blondeau, Sarah Kuylle, Sophie Holowacz, Agnès CosteAbstract:Candida albicans is an opportunistic pathogen that causes mucosal Gastrointestinal (GI) Candidiasis tightly associated with gut inflammatory status. The emergence of drug resistance, the side effects of currently available antifungals and the high frequency of recurrent Candidiasis indicate that new and improved therapeutics are needed. Probiotics have been suggested as a useful alternative for the management of Candidiasis. We demonstrated that oral administration of Lactobacillus gasseri LA806 alone or combined with Lactobacillus helveticus LA401 in Candida albicans-infected mice decrease the Candida colonization of the oesophageal and GI tract, highlighting a protective role for these strains in C. albicans colonization. Interestingly, the probiotic combination significantly modulates the composition of gut microbiota towards a protective profile and consequently dampens inflammatory and oxidative status in the colon. Moreover, we showed that L. helveticus LA401 and/or L. gasseri LA806 orient macrophages towards a fungicidal phenotype characterized by a C-type lectin receptors signature composed of Dectin-1 and Mannose receptor. Our findings suggest that the use of the LA401 and LA806 combination might be a promising strategy to manage GI Candidiasis and the inflammation it causes by inducing the intrinsic antifungal activities of macrophages. Thus, the probiotic combination is a good candidate for managing GI Candidiasis by inducing fungicidal functions in macrophages while preserving the GI integrity by modulating the microbiota and inflammation.
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IL-13 attenuates Gastrointestinal Candidiasis in normal and immunodeficient RAG-2(-/-) mice via peroxisome proliferator-activated receptor-gamma activation.
Journal of Immunology, 2008Co-Authors: Agnès Coste, Céline Lagane, Cédric Filipe, Hélène Authier, Amandine Galès, José Bernad, Victorine Douin-echinard, Jean-claude Lepert, Patricia Balard, Marie-denise LinasAbstract:We recently demonstrated that in vitro peroxisome proliferator-activated receptor-gamma (PPARgamma) activation of mouse peritoneal macrophages by IL-13 or PPARgamma ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2(-/-)) mice with natural and synthetic PPARgamma-specific ligands or with IL-13 decreases C. albicans colonization of the Gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARgamma antagonist, and are reduced in PPARgamma(+/-) mice. Overall, these data demonstrate that IL-13 or PPARgamma ligands attenuate C. albicans infection of the GI tract through PPARgamma activation and hence suggest that PPARgamma ligands may be of therapeutic value in esophageal and GI Candidiasis in immunocompromised patients.
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il 13 attenuates Gastrointestinal Candidiasis in normal and immunodeficient rag 2 mice via peroxisome proliferator activated receptor gamma activation
Journal of Immunology, 2008Co-Authors: Agnès Coste, Céline Lagane, Cédric Filipe, Hélène Authier, Amandine Galès, José Bernad, Jean-claude Lepert, Patricia Balard, Victorine Douinechinard, Marie-denise LinasAbstract:We recently demonstrated that in vitro peroxisome proliferator-activated receptor-gamma (PPARgamma) activation of mouse peritoneal macrophages by IL-13 or PPARgamma ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2(-/-)) mice with natural and synthetic PPARgamma-specific ligands or with IL-13 decreases C. albicans colonization of the Gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARgamma antagonist, and are reduced in PPARgamma(+/-) mice. Overall, these data demonstrate that IL-13 or PPARgamma ligands attenuate C. albicans infection of the GI tract through PPARgamma activation and hence suggest that PPARgamma ligands may be of therapeutic value in esophageal and GI Candidiasis in immunocompromised patients.
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IL-13 Attenuates Gastrointestinal Candidiasis in Normal and Immunodeficient RAG-2−/− Mice via Peroxisome Proliferator-Activated Receptor-γ Activation
Journal of immunology (Baltimore Md. : 1950), 2008Co-Authors: Agnès Coste, Céline Lagane, Cédric Filipe, Hélène Authier, Amandine Galès, José Bernad, Victorine Douin-echinard, Jean-claude Lepert, Patricia Balard, Marie-denise LinasAbstract:We recently demonstrated that in vitro peroxisome proliferator-activated receptor-gamma (PPARgamma) activation of mouse peritoneal macrophages by IL-13 or PPARgamma ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2(-/-)) mice with natural and synthetic PPARgamma-specific ligands or with IL-13 decreases C. albicans colonization of the Gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARgamma antagonist, and are reduced in PPARgamma(+/-) mice. Overall, these data demonstrate that IL-13 or PPARgamma ligands attenuate C. albicans infection of the GI tract through PPARgamma activation and hence suggest that PPARgamma ligands may be of therapeutic value in esophageal and GI Candidiasis in immunocompromised patients.
Ronald A Greenfield - One of the best experts on this subject based on the ideXlab platform.
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effect of abrogation of natural killer cell activity on the course of Candidiasis induced by intraperitoneal administration and Gastrointestinal Candidiasis in mice with severe combined immunodeficiency
Infection and Immunity, 1993Co-Authors: Ronald A Greenfield, V L Abrams, D L Crawford, Thomas L KuhlsAbstract:Candida albicans CFU per gram of tissue recovered from livers, spleens, and kidneys of 12 severe combined immunodeficiency (scid) and 12 BALB/c mice 5 days after intraperitoneal (i.p.) administration of 10(7) C. albicans cells were not significantly different. Nine scid mice given normal rabbit serum (NRS) as a control and eight scid mice given anti-asialo-GM1 (alpha-ASGM1) had C. albicans CFU per gram recovered from livers and spleens 1 week after i.p. administration of C. albicans that were not significantly different, despite virtual elimination of natural killer (NK) cell activity in mice treated with alpha-ASGM1. At 2 weeks after i.p. administration, despite significantly increased NK cell activity in eight infected NRS-treated scid mice and virtual elimination of NK cell activity by alpha-ASGM1 treatment of eight scid mice, C. albicans CFU per gram recovered from livers and kidneys were not significantly different. At 2 weeks after intragastric administration of 2 x 10(6) C. albicans cells, eight NRS- and eight alpha-ASGM1-treated scid mice had identical proportions colonized with C. albicans and similar C. albicans CFU per gram recovered from feces. There was no evidence of hematogenous dissemination in either group. Similar results were seen 1 week after intragastric administration of 10(7) C. albicans cells. We conclude that NK cell activity is increased by i.p. administration of C. albicans in scid mice, but nontheless, abrogation of NK cell activity is not associated with enhanced susceptibility to Candidiasis induced by i.p. administration and also is not associated with enhanced susceptibility to Gastrointestinal colonization or hematogenous dissemination after intragastric administration of C. albicans.
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Gastric colonization with Candida albicans.
Mycopathologia, 1993Co-Authors: Ronald A Greenfield, Wnedy A. JoyceAbstract:We adapted a rat model of Gastrointestinal Candidiasis for studies of in vivo gastric colonization withCandida albicans. Whereas normal rats cleared a single intragastric inoculum of 5×106C. albicans from the stomach within 4 hours, rats pretreated with chloramphenicol and gentamicin achieved stable gastric colonization for at least 5 days after administration of this inoculum. We next used this model to study host modifications hypothesized to alter gastric colonization. A first group received dilute HCl 4 hr before yeast inoculation, to induce acute superficial gastric erosions; another group was treated with glucocorticosteroid beginning 12 days before yeast inoculation; and another group received famotidine therapy beginning 3 days before yeast inoculation, to neutralize gastric acidity. Recovery of yeasts from stomachs was significantly different from the control group only in rats treated with steroids; greater colonization was found in the rats so treated. In a final group of experiments, we attempted to inhibit in vivo gastric colonization with yeasts by preincubation of yeasts in vitro with a polyclonal antiserum raised in rabbits against heat-killedC. albicans. We were not able to demonstrate inhibition of gastric colonization by preincubation with this antiserum in this model system.
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Gastric colonization withCandida albicans
Mycopathologia, 1993Co-Authors: Ronald A Greenfield, Wnedy A. JoyceAbstract:We adapted a rat model of Gastrointestinal Candidiasis for studies of in vivo gastric colonization with Candida albicans . Whereas normal rats cleared a single intragastric inoculum of 5×10^6 C. albicans from the stomach within 4 hours, rats pretreated with chloramphenicol and gentamicin achieved stable gastric colonization for at least 5 days after administration of this inoculum. We next used this model to study host modifications hypothesized to alter gastric colonization. A first group received dilute HCl 4 hr before yeast inoculation, to induce acute superficial gastric erosions; another group was treated with glucocorticosteroid beginning 12 days before yeast inoculation; and another group received famotidine therapy beginning 3 days before yeast inoculation, to neutralize gastric acidity. Recovery of yeasts from stomachs was significantly different from the control group only in rats treated with steroids; greater colonization was found in the rats so treated. In a final group of experiments, we attempted to inhibit in vivo gastric colonization with yeasts by preincubation of yeasts in vitro with a polyclonal antiserum raised in rabbits against heat-killed C. albicans . We were not able to demonstrate inhibition of gastric colonization by preincubation with this antiserum in this model system.
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Gastrointestinal Candidiasis in a murine model of severe combined immunodeficiency syndrome
Infection and Immunity, 1991Co-Authors: R Narayanan, W A Joyce, Ronald A GreenfieldAbstract:A murine model of severe combined immunodeficiency syndrome (scid mice) affords an opportunity to study the interaction of Candida albicans with a host lacking functional B- and T-cell mechanisms. We have previously reported no significant difference in yeast recovery after intravenous challenge of BALB/c mice and scid mice with C. albicans (S. Mahanty, R.A. Greenfield, W.A. Joyce, and P.W. Kincade, Infect. Immun. 56:3162-3166, 1988). In this study, we evaluate the course of Gastrointestinal Candidiasis after a single oral challenge with C. albicans. BALB/c and scid mice received H2O containing 10(6) C. albicans per ml for 16 h. Half the mice of each strain continuously received H2O containing 1 mg of tetracycline per ml. Stool samples were cultured for yeast twice weekly until they were negative three consecutive times or positive for 8 weeks. Mice were then sacrificed for quantitative cultures of liver, spleen, and kidneys. At eight weeks postinoculation, 2 of 13 BALB/c mice, 0 of 14 BALB/c mice receiving tetracycline, 6 of 12 scid mice, and 8 of 13 scid mice receiving tetracycline had positive stool cultures (P less than 0.05, likelihood ratio chi-square). Quantitative recovery of yeasts from stools was also higher in the scid mice. Cultures of liver, spleen, and kidneys wer negative in all BALB/c mice and essentially all negative in scid mice; a single colony was isolated from the kidney of one scid mouse and the liver of another scid mouse. We conclude that B cells and/or T cells and their products are important in Gastrointestinal colonization with C. albicans but that even in their absence, dissemination of infection from the Gastrointestinal tract does not consistently occur. Thus, other aspects of host defense must be critical in containing Gastrointestinal Candida colonization.
Hélène Authier - One of the best experts on this subject based on the ideXlab platform.
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oral administration of lactobacillus helveticus la401 and lactobacillus gasseri la806 combination attenuates oesophageal and Gastrointestinal Candidiasis and consequent gut inflammation in mice
Journal of Fungi, 2021Co-Authors: Hélène Authier, Marie Salon, Mouna Rahabi, Benedicte Bertrand, Claude Blondeau, Sarah Kuylle, Sophie Holowacz, Agnès CosteAbstract:Candida albicans is an opportunistic pathogen that causes mucosal Gastrointestinal (GI) Candidiasis tightly associated with gut inflammatory status. The emergence of drug resistance, the side effects of currently available antifungals and the high frequency of recurrent Candidiasis indicate that new and improved therapeutics are needed. Probiotics have been suggested as a useful alternative for the management of Candidiasis. We demonstrated that oral administration of Lactobacillus gasseri LA806 alone or combined with Lactobacillus helveticus LA401 in Candida albicans-infected mice decrease the Candida colonization of the oesophageal and GI tract, highlighting a protective role for these strains in C. albicans colonization. Interestingly, the probiotic combination significantly modulates the composition of gut microbiota towards a protective profile and consequently dampens inflammatory and oxidative status in the colon. Moreover, we showed that L. helveticus LA401 and/or L. gasseri LA806 orient macrophages towards a fungicidal phenotype characterized by a C-type lectin receptors signature composed of Dectin-1 and Mannose receptor. Our findings suggest that the use of the LA401 and LA806 combination might be a promising strategy to manage GI Candidiasis and the inflammation it causes by inducing the intrinsic antifungal activities of macrophages. Thus, the probiotic combination is a good candidate for managing GI Candidiasis by inducing fungicidal functions in macrophages while preserving the GI integrity by modulating the microbiota and inflammation.
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IL-13 attenuates Gastrointestinal Candidiasis in normal and immunodeficient RAG-2(-/-) mice via peroxisome proliferator-activated receptor-gamma activation.
Journal of Immunology, 2008Co-Authors: Agnès Coste, Céline Lagane, Cédric Filipe, Hélène Authier, Amandine Galès, José Bernad, Victorine Douin-echinard, Jean-claude Lepert, Patricia Balard, Marie-denise LinasAbstract:We recently demonstrated that in vitro peroxisome proliferator-activated receptor-gamma (PPARgamma) activation of mouse peritoneal macrophages by IL-13 or PPARgamma ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2(-/-)) mice with natural and synthetic PPARgamma-specific ligands or with IL-13 decreases C. albicans colonization of the Gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARgamma antagonist, and are reduced in PPARgamma(+/-) mice. Overall, these data demonstrate that IL-13 or PPARgamma ligands attenuate C. albicans infection of the GI tract through PPARgamma activation and hence suggest that PPARgamma ligands may be of therapeutic value in esophageal and GI Candidiasis in immunocompromised patients.
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il 13 attenuates Gastrointestinal Candidiasis in normal and immunodeficient rag 2 mice via peroxisome proliferator activated receptor gamma activation
Journal of Immunology, 2008Co-Authors: Agnès Coste, Céline Lagane, Cédric Filipe, Hélène Authier, Amandine Galès, José Bernad, Jean-claude Lepert, Patricia Balard, Victorine Douinechinard, Marie-denise LinasAbstract:We recently demonstrated that in vitro peroxisome proliferator-activated receptor-gamma (PPARgamma) activation of mouse peritoneal macrophages by IL-13 or PPARgamma ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2(-/-)) mice with natural and synthetic PPARgamma-specific ligands or with IL-13 decreases C. albicans colonization of the Gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARgamma antagonist, and are reduced in PPARgamma(+/-) mice. Overall, these data demonstrate that IL-13 or PPARgamma ligands attenuate C. albicans infection of the GI tract through PPARgamma activation and hence suggest that PPARgamma ligands may be of therapeutic value in esophageal and GI Candidiasis in immunocompromised patients.
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IL-13 Attenuates Gastrointestinal Candidiasis in Normal and Immunodeficient RAG-2−/− Mice via Peroxisome Proliferator-Activated Receptor-γ Activation
Journal of immunology (Baltimore Md. : 1950), 2008Co-Authors: Agnès Coste, Céline Lagane, Cédric Filipe, Hélène Authier, Amandine Galès, José Bernad, Victorine Douin-echinard, Jean-claude Lepert, Patricia Balard, Marie-denise LinasAbstract:We recently demonstrated that in vitro peroxisome proliferator-activated receptor-gamma (PPARgamma) activation of mouse peritoneal macrophages by IL-13 or PPARgamma ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2(-/-)) mice with natural and synthetic PPARgamma-specific ligands or with IL-13 decreases C. albicans colonization of the Gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARgamma antagonist, and are reduced in PPARgamma(+/-) mice. Overall, these data demonstrate that IL-13 or PPARgamma ligands attenuate C. albicans infection of the GI tract through PPARgamma activation and hence suggest that PPARgamma ligands may be of therapeutic value in esophageal and GI Candidiasis in immunocompromised patients.
Jean-claude Lepert - One of the best experts on this subject based on the ideXlab platform.
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IL-13 attenuates Gastrointestinal Candidiasis in normal and immunodeficient RAG-2(-/-) mice via peroxisome proliferator-activated receptor-gamma activation.
Journal of Immunology, 2008Co-Authors: Agnès Coste, Céline Lagane, Cédric Filipe, Hélène Authier, Amandine Galès, José Bernad, Victorine Douin-echinard, Jean-claude Lepert, Patricia Balard, Marie-denise LinasAbstract:We recently demonstrated that in vitro peroxisome proliferator-activated receptor-gamma (PPARgamma) activation of mouse peritoneal macrophages by IL-13 or PPARgamma ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2(-/-)) mice with natural and synthetic PPARgamma-specific ligands or with IL-13 decreases C. albicans colonization of the Gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARgamma antagonist, and are reduced in PPARgamma(+/-) mice. Overall, these data demonstrate that IL-13 or PPARgamma ligands attenuate C. albicans infection of the GI tract through PPARgamma activation and hence suggest that PPARgamma ligands may be of therapeutic value in esophageal and GI Candidiasis in immunocompromised patients.
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il 13 attenuates Gastrointestinal Candidiasis in normal and immunodeficient rag 2 mice via peroxisome proliferator activated receptor gamma activation
Journal of Immunology, 2008Co-Authors: Agnès Coste, Céline Lagane, Cédric Filipe, Hélène Authier, Amandine Galès, José Bernad, Jean-claude Lepert, Patricia Balard, Victorine Douinechinard, Marie-denise LinasAbstract:We recently demonstrated that in vitro peroxisome proliferator-activated receptor-gamma (PPARgamma) activation of mouse peritoneal macrophages by IL-13 or PPARgamma ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2(-/-)) mice with natural and synthetic PPARgamma-specific ligands or with IL-13 decreases C. albicans colonization of the Gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARgamma antagonist, and are reduced in PPARgamma(+/-) mice. Overall, these data demonstrate that IL-13 or PPARgamma ligands attenuate C. albicans infection of the GI tract through PPARgamma activation and hence suggest that PPARgamma ligands may be of therapeutic value in esophageal and GI Candidiasis in immunocompromised patients.
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IL-13 Attenuates Gastrointestinal Candidiasis in Normal and Immunodeficient RAG-2−/− Mice via Peroxisome Proliferator-Activated Receptor-γ Activation
Journal of immunology (Baltimore Md. : 1950), 2008Co-Authors: Agnès Coste, Céline Lagane, Cédric Filipe, Hélène Authier, Amandine Galès, José Bernad, Victorine Douin-echinard, Jean-claude Lepert, Patricia Balard, Marie-denise LinasAbstract:We recently demonstrated that in vitro peroxisome proliferator-activated receptor-gamma (PPARgamma) activation of mouse peritoneal macrophages by IL-13 or PPARgamma ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2(-/-)) mice with natural and synthetic PPARgamma-specific ligands or with IL-13 decreases C. albicans colonization of the Gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARgamma antagonist, and are reduced in PPARgamma(+/-) mice. Overall, these data demonstrate that IL-13 or PPARgamma ligands attenuate C. albicans infection of the GI tract through PPARgamma activation and hence suggest that PPARgamma ligands may be of therapeutic value in esophageal and GI Candidiasis in immunocompromised patients.
