Effet chez le porcelet d'une exposition à un régime co-contaminé en ...

TRAVAIL EXPERIMENTAL1998), were greatly reduced in liver and thereby, could confirm the inflammatory state in pigletsexposed to FB1. By contrast, HFB1 administration did not modulate the cytokines expression as muchas FB1 did, and to our knowledge this is the first report on the effect of HFB1 on cytokines in liver.The lack of toxicity in liver after HFB1 exposure is in agreement with some authors (Collins et al.,2006; Howard et al., 2002; Voss et al., 2009), but also in discordance with others (Hendrich et al.,1993; Voss et al., 1996; Voss et al., 1998). Nonetheless, in these controversial studies, it is importantto clarify that the toxicity was only demonstrated in animals exposed to nixtamalized culture materialand not to pure HFB1. That’s why, it was suggested (Kim et al., 2003; Park et al., 2004; Seiferlein etal., 2007; Burns et al., 2008; Voss et al., 2009) that these effects were mediated by residual or“hidden” FB1 (matrix bound forms not detected by HPLC) remaining in the nixtamalizedpreparations, rather than HFB1.We also determined the potential toxicity of these compounds on the intestine. Indeed, as thegastrointestinal tract is a primary site of mycotoxins exposure and that FB1 has been also reported toexert its toxicity, through the ceramide synthase inhibition, in the intestine (Enongene et al., 2000;Loiseau et al., 2007), evaluation of HFB1 effects on intestine was necessary. Following ingestion ofcontaminated food or feed, intestinal epithelial cells could be exposed to a high concentration oftoxicants, potentially affecting intestinal functions. Some studies focused on the bowel, but most ofthem concern effects of HFB1 on intestinal cell lines by assessing the number of viable cells, HFB1acylation or sphingoid bases content (Schmelz et al., 1998; Humpf et al., 1998; Seiferlein et al., 2007).In the current study, HFB1 ingestion did not alter the intestinal integrity in the different segmentsexamined, as shown by the villi morphometry and the lesion scores. Among lesions, villi atrophy andfusion were evaluated. Occurrence of these lesions was considerably high in the intestines exposedto FB1, especially in the second part of the small intestine. These findings are in agreement with thevillous fusion and atrophy observed in the intestine of pigs treated with 30 ppm FB1 (Piva et al.,2005) and in the intestine of chicks fed with 61-546 ppm FB1 (Javed et al., 2005). In addition, a reporton human consumption of moldy maize (containing fumonisins) resulted in abdominal pain,borborygmi, and diarrhea (Bhat et al., 1997). Therefore, it can be suggested that on contrary to FB1,HFB1 consumption would not lead to impairment of the intestinal absorption of nutrients.The intestine is also an immune privileged site where immunoregulatory mechanismssimultaneously defend against pathogens but also preserve tissues homeostasis to avoid immunemediatedpathology in response to environmental challenges (Ramiro-Puig et al., 2008). To assessthe intestinal immunity following exposure to FB1 and HFB1, we focused on different sections of thejejunum, and on ileum and mesenteric lymph nodes (MLN) as well. In contrast to the jejunum, whichprovides a local response, the ileum containing Peyer’s patches and MLN take part from the gut-138