These are not the final page numbersMol. Nutr. Food Res. 2011, 55, 1–11 11[21] Leslie, J. F., Plattner, R. D., Desjardins, A. E., Klittich, C. J. R.,Fumonisin B1 production by strains from differ<strong>en</strong>t matingpopulations of Gibberella-Fujikuroi (Fusarium SectionLiseola). Phytopathology 1992, 82, 341–345.[22] Sulyok, M., Krska, R., Schuhmacher, R., A liquid chromatography/tandemmass spectrometric multi-my<strong>co</strong>toxinmethod for the quantification of 87 analytes and itsapplication to semi-quantitative scre<strong>en</strong>ing of moldyfood samp<strong>le</strong>s. Anal. Bioanal. Chem. 2007, 389,1505–1523.[23] Kolf-Clauw, M., Castellote, J., Joly, B., Bourges-Abella, N.et al., Developm<strong>en</strong>t of a pig jej<strong>un</strong>al explant culture forstudying the gastrointestinal toxicity of the my<strong>co</strong>toxindeoxyniva<strong>le</strong>nol: histopathological analysis. Toxi<strong>co</strong>l. Vitro2009, 23, 1580–1584.[24] Makino, H., Togo, S., Kubota, T., Morioka, D. et al., A goodmodel of hepatic failure after excessive hepatectomy inmice. J. Surg. Res. 2005, 127, 171–176.[25] Taranu, I., Marin, D. E., Bouhet, S., Pasca<strong>le</strong>, F. et al.,My<strong>co</strong>toxin fumonisin B-1 alters the cytokine profi<strong>le</strong> anddecreases the vaccinal antibody titer in pigs. Toxi<strong>co</strong>l. Sci.2005, 84, 301–307.[26] Meissonnier, G. M., Pinton, P., Laffitte, J., Cossalter, A. M.et al., Imm<strong>un</strong>otoxicity of aflatoxin B1: Impairm<strong>en</strong>t of the cellmediatedresponse to vaccine antig<strong>en</strong> and modulation ofcytokine expression. Toxi<strong>co</strong>l. Appl. Pharma<strong>co</strong>l. 2008, 231,142–149.[27] Devri<strong>en</strong>dt, B., Gallois, M., Verdonck, F., Wache, Y. et al.,The food <strong>co</strong>ntaminant fumonisin B-1 reduces thematuration of porcine CD11R1(1) intestinal antig<strong>en</strong>pres<strong>en</strong>ting cells and antig<strong>en</strong>-specific imm<strong>un</strong>e responses,<strong>le</strong>ading to a prolonged intestinal ETEC infection. Vet. Res.2009, 40, 40.[28] Voss, K. A., Ri<strong>le</strong>y, R. T., Norred, W. P., Ba<strong>co</strong>n, C. W. et al., Anoverview of rod<strong>en</strong>t toxicities: liver and kidney effects offumonisins and Fusarium moniliforme. Environ. HealthPerspect. 2001, 109, 259–266.[29] Broomhead, J. N., Ledoux, D. R., Bermudez, A. J., Rottinghaus,G. E., Chronic effects of fumonisin B-1 in broi<strong>le</strong>rsand turkeys fed dietary treatm<strong>en</strong>ts to market age. Poult. Sci.2002, 81, 56–61.[30] Eti<strong>en</strong>ne, M., Wache, Y., in: Oswald, I. P., Taranu, I. (Eds.),My<strong>co</strong>toxins in Farm Animals, Research Signpost, Kerala2008, pgs. 113–130.[31] Odhav, B., Adam, J. K., Bhoola, K. D., Modulating effects offumonisin B1 and ochratoxin A on <strong>le</strong>ukocytes andmess<strong>en</strong>ger cytokines of the human imm<strong>un</strong>e system. Int.Imm<strong>un</strong>opharma<strong>co</strong>l. 2008, 8, 799–809.[32] Bergsjo, B., Langseth, W., Nafstad, I., Jans<strong>en</strong>, J. H., Lars<strong>en</strong>,H. J. S., The effects of naturally deoxyniva<strong>le</strong>nol-<strong>co</strong>ntaminatedoats on the clinical <strong>co</strong>ndition, blood parameters,performance and carcass <strong>co</strong>mposition of growing pigs. Vet.Res. Comm<strong>un</strong>. 1993, 17, 283–294.[33] Rotter, B. A., Thompson, B. K., Lessard, M., Effects ofdeoxyniva<strong>le</strong>nol-<strong>co</strong>ntaminated diet on performance andblood parameters in growing swine. Can. J. Anim. Sci.1995, 75, 297–302.[34] Zielonka, L., Wisniewska, M., Gajecka, M., Obremski, K.,Gajecki, M., Influ<strong>en</strong>ce of low doses of deoxyniva<strong>le</strong>nol onhistopathology of se<strong>le</strong>cted organs of pigs. Pol. J. Vet. Sci.2009, 12, 89–95.[35] Ch<strong>en</strong>, F., Ma, Y. L., Xue, C. Y., Ma, J. Y. et al., The <strong>co</strong>mbinationof deoxyniva<strong>le</strong>nol and zeara<strong>le</strong>none at permitted feed<strong>co</strong>nc<strong>en</strong>trations causes serious physiological effects inyo<strong>un</strong>g pigs. J. Vet. Sci. 2008, 9, 39–44.[36] Tiemann, U., Brussow, K. P., Kuch<strong>en</strong>meister, U., Jonas, L.et al., Influ<strong>en</strong>ce of diets with cereal grains <strong>co</strong>ntaminated bygraded <strong>le</strong>vels of two Fusarium toxins on se<strong>le</strong>cted <strong>en</strong>zymaticand histological parameters of liver in gilts. Food Chem.Toxi<strong>co</strong>l. 2006, 44, 1228–1235.[37] Pinton, P., Nougayrede, J. P., Del Rio, J. C., Mor<strong>en</strong>o, C.et al., The food <strong>co</strong>ntaminant deoxyniva<strong>le</strong>nol, decreasesintestinal barrier permeability and reduces claudin expression.Toxi<strong>co</strong>l. Appl. Pharma<strong>co</strong>l. 2009, 237, 41–48.[38] Marin, D. E., Gouze, M. E., Taranu, I., Oswald, I. P., FumonisinB1 alters cell cyc<strong>le</strong> progression and inter<strong>le</strong>ukin-2synthesis in swine peripheral blood mononuc<strong>le</strong>ar cells.Mol. Nutr. Food Res. 2007, 51, 1406–1412.[39] Bimczok, D., Doll, S., Rau, H., Goyarts, T. et al., The Fusariumtoxin deoxyniva<strong>le</strong>nol disrupts ph<strong>en</strong>otype and f<strong>un</strong>ctionof monocyte-derived d<strong>en</strong>dritic cells in vivo and in vitro.Imm<strong>un</strong>obiology 2007, 212, 655–666.[40] Wache, Y. J., Hbabi-Haddioui, L., Guzylack-Piriou, L.,Belkhelfa, H. et al., The my<strong>co</strong>toxin Deoxyniva<strong>le</strong>nol inhibitsthe cell surface expression of activation markers in humanmacrophages. Toxi<strong>co</strong>logy 2009, 262, 239–244.[41] Loiseau, N., Debrauwer, L., Sambou, T., Bouhet, S. et al.,Fumonisin B-1 exposure and its se<strong>le</strong>ctive effect on porcinejej<strong>un</strong>al segm<strong>en</strong>t: sphingolipids, gly<strong>co</strong>lipids and transepithelialpassage disturbance. Biochem. Pharma<strong>co</strong>l. 2007,74, 144–152.[42] Soriano, J. M., Gonza<strong>le</strong>z, L., Catala, A. I., Mechanism ofaction of sphingolipids and their metabolites in the toxicityof fumonisin B1. Prog. Lipid Res. 2005, 44, 345–356.[43] Furuya, H., Ohkawara, S., Nagashima, K., Asanuma, N.,Hino, T., Dietary sphingomyelin al<strong>le</strong>viates experim<strong>en</strong>talinflammatory bowel disease in mice. Int. J. Vitam. Nutr.Res. 2008, 78, 41–49.[44] Pinelli, E., Poux, N., Garr<strong>en</strong>, L., Pipy, B. et al., Activation ofmitog<strong>en</strong>-activated protein kinase by fumonisin B-1 stimulatescPLA(2) phosphorylation, the arachidonic acidcascade and cAMP production. Carcinog<strong>en</strong>esis 1999, 20,1683–1688.[45] Dong, C., Davis, R. J., Flavell, R. A., MAP kinases in theimm<strong>un</strong>e response. Annu. Rev. Imm<strong>un</strong>ol. 2002, 20, 55–72.[46] Pinton, P., Braicu, C., Nougayrede, J. P., Laffitte, J. et al.,Deoxyniva<strong>le</strong>nol impairs porcine intestinal barrier f<strong>un</strong>ctionand decreases the protein expression of claudin-4 through amitog<strong>en</strong> activated protein kinase dep<strong>en</strong>d<strong>en</strong>t mechanism.J. Nutr. 2010, 140, 1956–1962.& 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheimwww.mnf-journal.<strong>co</strong>m
TRAVAIL EXPERIMENTAL2. Toxicité in vivo du déoxynivalénol et des fumonisines, seuls ou <strong>en</strong><strong>co</strong>mbinaison sur la morphologie et la réponse loca<strong>le</strong> de l’intestinL’expérim<strong>en</strong>tation anima<strong>le</strong> prés<strong>en</strong>tée dans la première étude a éga<strong>le</strong>m<strong>en</strong>t fait l’objet derecherches sur l’effet des quatre régimes sur l’intestin. Des échantillons d’intestin grê<strong>le</strong> ont étépré<strong>le</strong>vés lors de l’autopsie des animaux, et des analyses histologiques et imm<strong>un</strong>ologiques ont étéréalisées.Les résultats histologiques ont montré <strong>un</strong>e augm<strong>en</strong>tation du nombre de lésions après l’ingestiondes my<strong>co</strong>toxines, au niveau du jéj<strong>un</strong>um et de l’iléon. L’effet observé sur <strong>le</strong>s cellu<strong>le</strong>s <strong>en</strong> mitosepourrait expliquer l’aplatissem<strong>en</strong>t des villosités dans la partie jéj<strong>un</strong>a<strong>le</strong>. Néanmoins, ces <strong>co</strong>nclusionssur <strong>le</strong>s analyses histologiques ont été principa<strong>le</strong>m<strong>en</strong>t <strong>co</strong>nfirmées pour <strong>le</strong> régime mono-<strong>co</strong>ntaminéavec <strong>le</strong> DON. Et il semb<strong>le</strong>rait que la prés<strong>en</strong>ce de FB ait <strong>un</strong> effet antagoniste sur l’effet du DON dans <strong>le</strong>régime <strong>co</strong>-<strong>co</strong>ntaminé. Ce même type d’interaction a été observé sur la diminution du nombre decellu<strong>le</strong>s caliciformes dans <strong>le</strong> jéj<strong>un</strong>um.L’analyse de l’expression des cytokines par RT-PCR temps réel a montré de manière intéressante,<strong>un</strong>e augm<strong>en</strong>tation du niveau des ARN dans <strong>le</strong> jéj<strong>un</strong>um et l’iléon. L’augm<strong>en</strong>tation de l’IL-6 causée par<strong>le</strong> DON pourrait être <strong>co</strong>rrélée à l’élévation du titre <strong>en</strong> IgA spécifiques observée dans la premièreétude. L’augm<strong>en</strong>tation généra<strong>le</strong> des ARNs <strong>co</strong>dant pour diverses cytokines tout au long de l’intestingrê<strong>le</strong>, suggère <strong>un</strong> état inflammatoire chronique suite à l’<strong>exposition</strong> <strong>co</strong>ntinue aux régimes <strong>co</strong>ntaminésp<strong>en</strong>dant <strong>le</strong>s cinq semaines. Dans ce s<strong>en</strong>s, il a été reporté dans la littérature que lors d’inflammationsdigestives chroniques, l’expression exacerbée de certaines cytokines (IL-1β, TNF-α et IFN-γ) induisait<strong>un</strong>e plus grande perméabilité intestina<strong>le</strong>. Basé sur ces observations et sur <strong>le</strong>s réc<strong>en</strong>ts travaux d<strong>en</strong>otre équipe sur l’altération de l’expression de protéines de jonctions par <strong>le</strong> DON, nous avons ainsimontré qu’in vivo, <strong>le</strong>s régimes <strong>co</strong>ntaminés diminuai<strong>en</strong>t l’expression protéique de l’E-cadhérine et del’occludine au niveau de l’iléon; <strong>un</strong> effet additif étant obt<strong>en</strong>u pour <strong>le</strong> régime <strong>co</strong>-<strong>co</strong>ntaminé.107
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AUTEUR : Bertrand GRENIERTITRE : Ef
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REMERCIEMENTSLe travail ici présen
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J’ai une pensée particulière po
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Grenier, B., Loureiro-Bracarense, A
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TABLE DES MATIERES ................
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LISTE DES ABREVIATIONSAFAflatoxineD
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FIGURES ET TABLEAUXFigure 1 : Mycot
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INTRODUCTION8
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INTRODUCTIONCONTEXTE DE L’ETUDELe
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INTRODUCTIONElle se présentait sou
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INTRODUCTIONl’utilisation de ce m
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INTRODUCTION1. Les mycotoxines : g
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INTRODUCTIONc) La zéaralénone (vo
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INTRODUCTIONleucoencéphalomalacies
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INTRODUCTIONMycotoxins co-contamina
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INTRODUCTIONINTRODUCTIONFood safety
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INTRODUCTIONCHARACTERIZATION OF THE
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Quail(140 d)AF-FBRabbit(21 d)AF-FBR
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INTRODUCTIONdue to the ingestion of
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Table 2 : Interaction between Aflat
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(49 d) - RW-L ↗- Ab SRBC ↘- RW-
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INTRODUCTIONb) effects AF and OTA o
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INTRODUCTIONThe depletion of lympho
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AF-T2Chicken 0.3 - 3.0(35 d)AF-T2Ra
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INTRODUCTIONonly seen in birds give
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(30 d) 2AF-RUBGuinea pig 0.02 bw -(
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INTRODUCTIONbetween AF and CPA on t
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(21 day) - RBC, hemoglobin ↗- AST
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INTRODUCTIONII. INTERACTIONS BETWEE
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INTRODUCTIONwhereas in the experime
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INTRODUCTION2.2) TCT type A and BTw
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Table 6 : Interaction between Ochra
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T2-CPAChicken(28 d)T2-CPAChicken(21
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INTRODUCTIONexposed group (Brown et
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INTRODUCTION2.3) Interaction betwee
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INTRODUCTIONeffects in comparison t
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INTRODUCTION3. Procédés de décon
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INTRODUCTIONPhysical and chemical m
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INTRODUCTIONINTRODUCTIONConsumption
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INTRODUCTIONmm screen shows that fr
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INTRODUCTIONseparate the grain into
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Table 7 : toxicological evaluation
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INTRODUCTIONextrusion parameters ra
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Figure 14 :Illustrations de la proc
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Figure 15 :Plan expérimental de la
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TRAVAIL EXPERIMENTAL4) Analyses du
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TRAVAIL EXPERIMENTAL9) Analyses sta
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TRAVAIL EXPERIMENTALRESULTATS1) Eff
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TRAVAIL EXPERIMENTAL2) Effet des ag
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TRAVAIL EXPERIMENTALb,cca,ba,b,da,d
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TRAVAIL EXPERIMENTALL’exposition
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Figure 21 : Effet de l’exposition
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1,41,21,00,80,60,40,20,0IL‐8a,cc
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TRAVAIL EXPERIMENTALDISCUSSIONLes o
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TRAVAIL EXPERIMENTALœdèmes pulmon
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DISCUSSIONGENERALE160
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DISCUSSION GENERALEDans ce travail
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DISCUSSION GENERALEdes vaches laiti
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Tableau 24 : Analyse de denrées ag
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DISCUSSION GENERALEet al., 2008b).
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DISCUSSION GENERALE• une réactio
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DISCUSSION GENERALE2. Les systèmes
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DISCUSSION GENERALEMycoplasma agala
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DISCUSSION GENERALEoptimale. Les au
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DISCUSSION GENERALEsphingomyéline
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DISCUSSION GENERALEsignalisation ce
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DISCUSSION GENERALEL’IMMUNITÉ IN
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DISCUSSION GENERALEplus spécifique
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DISCUSSION GENERALEsouligner que le
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DISCUSSION GENERALELA CARBOXYLESTER
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DISCUSSION GENERALEde HFB1. Toutefo
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CONCLUSIONS184
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CONCLUSIONSLes effets d’expositio
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CONCLUSIONSest utilisée lorsque la
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REFERENCES BIBLIOGRAPHIQUESAABDEL-W
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REFERENCES BIBLIOGRAPHIQUESBHANDARI
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REFERENCES BIBLIOGRAPHIQUESCASADO,
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REFERENCES BIBLIOGRAPHIQUESDEGIRMEN
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REFERENCES BIBLIOGRAPHIQUESETIENNE,
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REFERENCES BIBLIOGRAPHIQUESGRENIER,
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REFERENCES BIBLIOGRAPHIQUESHERZALLA
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REFERENCES BIBLIOGRAPHIQUESKERKADI,
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REFERENCES BIBLIOGRAPHIQUESKUMAR, M
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REFERENCES BIBLIOGRAPHIQUESMARZOCCO
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REFERENCES BIBLIOGRAPHIQUESODHAV, B
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REFERENCES BIBLIOGRAPHIQUESPFOHL-LE
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REFERENCES BIBLIOGRAPHIQUESREFAI, M
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REFERENCES BIBLIOGRAPHIQUESSCHWARTZ
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REFERENCES BIBLIOGRAPHIQUESSWANSON,
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REFERENCES BIBLIOGRAPHIQUESVEKIRU,
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REFERENCES BIBLIOGRAPHIQUESYAN, D.,
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