Dataset Information

Effects of a Fusarium Toxin-Contaminated Maize Treated with Sodium Sulfite on Male Piglets in the Presence of an LPS-Induced Acute Inflammation.

ABSTRACT: We investigated the effects of feeding sodium sulfite (SoS) treated uncontaminated and Fusarium contaminated maize in a porcine lipopolysaccharide (LPS) challenge model. Eighty piglets (7.59 ± 0.92 kg body weight [BW]) were equally assigned to one of four experimental diets containing 10% maize, either uncontaminated and untreated (CON-, 0.09 mg deoxynivalenol [DON]/kg diet) or uncontaminated and SoS-treated (CON+, wet-preserved with 5 g SoS/kg maize; 0.05 mg DON/kg diet), or prepared with 10% of a Fusarium contaminated maize containing mainly deoxynivalenol (DON), either contaminated and untreated (FUS-, 5.36 mg DON/kg diet), or contaminated and SoS-treated (FUS+, wet-preserved with 5 g SoS/kg maize; 0.83 mg DON/kg diet). At day 42 of experiment, ten pigs of each group were injected intraperitoneally with either 7.5 µg LPS/kg BW or placebo (0.9% NaCl). At 120 min after injection, blood samples were collected to analyse TNF-?, hematological profile, clinical biochemistry as well as the redox status. A significant increase in body temperature and cytokine TNF-? concentration was observed in the LPS-injected piglets. Results for hematology, clinical chemistry and redox status indicate no effects of SoS treatment, with exception of neutrophil counts being significantly more pronounced after feeding the SoS treated FUS maize. In conclusion, SoS treatment of maize did not modulate the LPS-induced acute inflammation.

SUBMITTER: Tran AT

PROVIDER: S-EPMC6215154 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Effects of a <i>Fusarium</i> Toxin-Contaminated Maize Treated with Sodium Sulfite on Male Piglets in the Presence of an LPS-Induced Acute Inflammation.

Tran Anh-Tuan AT Kluess Jeannette J Berk Andreas A Paulick Marleen M Frahm Jana J Schatzmayr Dian D Kersten Susanne S Dänicke Sven S

Toxins 20181018 10

We investigated the effects of feeding sodium sulfite (SoS) treated uncontaminated and <i>Fusarium</i> contaminated maize in a porcine lipopolysaccharide (LPS) challenge model. Eighty piglets (7.59 ± 0.92 kg body weight [BW]) were equally assigned to one of four experimental diets containing 10% maize, either uncontaminated and untreated (CON-, 0.09 mg deoxynivalenol [DON]/kg diet) or uncontaminated and SoS-treated (CON+, wet-preserved with 5 g SoS/kg maize; 0.05 mg DON/kg diet), or prepared wit ...[more]

PMID: 30340332

Similar Datasets

Project description:Exposure to (bi)sulfite (HSO3-) and sulfite (SO32-) has been shown to induce a wide range of adverse reactions in sensitive individuals. Studies have shown that peroxidase-catalyzed oxidation of (bi)sulfite leads to formation of several reactive free radicals, such as sulfur trioxide anion (.SO3-), peroxymonosulfate (-O3SOO.), and especially the sulfate (SO4. -) anion radicals. One such peroxidase in neutrophils is myeloperoxidase (MPO), which has been shown to form protein radicals. Although formation of (bi)sulfite-derived protein radicals is documented in isolated neutrophils, its involvement and role in in vivo inflammatory processes, has not been demonstrated. Therefore, we aimed to investigate (bi)sulfite-derived protein radical formation and its mechanism in LPS aerosol-challenged mice, a model of non-atopic asthma. Using immuno-spin trapping to detect protein radical formation, we show that, in the presence of (bi)sulfite, neutrophils present in bronchoalveolar lavage and in the lung parenchyma exhibit, MPO-catalyzed oxidation of MPO to a protein radical. The absence of radical formation in LPS-challenged MPO- or NADPH oxidase-knockout mice indicates that sulfite-derived radical formation is dependent on both MPO and NADPH oxidase activity. In addition to its oxidation by the MPO-catalyzed pathway, (bi)sulfite is efficiently detoxified to sulfate by the sulfite oxidase (SOX) pathway, which forms sulfate in a two-electron oxidation reaction. Since SOX activity in rodents is much higher than in humans, to better model sulfite toxicity in humans, we induced SOX deficiency in mice by feeding them a low molybdenum diet with tungstate. We found that mice treated with the SOX deficiency diet prior to exposure to (bi)sulfite had much higher protein radical formation than mice with normal SOX activity. Altogether, these results demonstrate the role of MPO and NADPH oxidase in (bi)sulfite-derived protein radical formation and show the involvement of protein radicals in a mouse model of human lung disease.

Project description:Background:Following the intake of Fusarium mycotoxin-contaminated feed, small intestines may be exposed to high levels of toxic substances that can potentially damage intestinal functions in livestock. It is well known that Fusarium mycotoxins will lead a breakdown of the normally impeccable epithelial barrier, resulting in the development of a "leaky" gut. H2 administration with different methods has been proved definitely potentials to prevent serious intestinal diseases. The goal of this study is to investigate the roles of lactulose (LAC) and hydrogen-rich water (HRW) in preventing intestinal dysfunction in piglets fed Fusarium mycotoxin-contaminated feed. Methods:A total of 24 female piglets were evenly assigned to 4 groups: negative control (NC) group, mycotoxin-contaminated (MC) feed group, MC feed with LAC treatment (MC?+?LAC), and MC feed with HRW treatment (MC?+?HRW), respectively. Piglets in the NC group were fed uncontaminated control diet, while remaining piglets were fed Fusarium mycotoxin-contaminated diet. For the NC and MC groups, 10?mL/kg body weight (BW) of hydrogen-free water (HFW) was orally administrated to piglets twice daily; while in the MC?+?LAC and MC?+?HRW groups, piglets were treated with the same dose of LAC solution (500?mg/kg BW) and HRW twice daily, respectively. On d 25, serum was collected and used for biochemical analysis. Intestinal tissues were sampled for morphological examination as well as relative genes and protein expression analysis. Results:Our data showed that Fusarium mycotoxins induced higher serum diamine oxidase (DAO) activities (P?< 0.05), D-lactic acid levels (P?< 0.01), and endotoxin status (P?< 0.01), lower villus height (P?< 0.01) and ratio of villus height to crypt depth (P?< 0.05) in small intestine, greater apoptosis index and higher mRNA expression related to tight junctions (P?< 0.05). In addition, the distribution and down-regulation of claudin-3 (CLDN3) protein in the small intestinal was also observed. As expected, oral administrations of HRW and LAC were found to remarkably provide beneficial effects against Fusarium mycotoxin-induced apoptosis and intestinal leaking. Moreover, either HRW or LAC treatments were also revealed to prevent abnormal intestinal morphological changes, disintegrate tight junctions, and restore the expression and distribution of CLDN3 protein in the small intestinal mucosal layer in female piglets that were fed Fusarium mycotoxins contaminated diet. Conclusions:Our data suggest that orally administrations of HRW and LAC result in less Fusarium mycotoxin-induced apoptosis and leak in the small intestine. Either HRW or LAC treatments could prevent the abnormal changes of intestinal morphology and molecular response of tight junctions as well as restore the distribution and expression of CLDN3 protein of small intestinal mucosa layer in female piglets that were fed Fusarium mycotoxins contaminated diet.

Project description:BackgroundGibberella stalk rot caused by Fusarium graminearum is one of the most destructive soil-borne diseases of maize (Zea mays L.). Chemical means of controlling Gibberella stalk rot are not very effective; development of highly resistant hybrids is the best choice for disease control. Hence, understanding of the molecular basis underlying maize resistance against Gibberella stalk rot would undoubtedly facilitate the resistance breeding for stalk rot.ResultsTwo quantitative trait loci (QTL), qRfg1 and qRfg2, conferring resistance to Gibberella stalk rot were detected in our previous study. Three near-isogenic lines (NILs) of maize with either qRfg1 (NIL1) or qRfg2 (NIL2), or neither (NIL3) were generated and subjected to RNA sequencing to study the transcriptional changes after F. graminearum inoculation at 0 (control), 6, and 18 h post-inoculation (hpi). In total, 536,184,652 clean reads were generated, and gene expression levels were calculated using FPKM (fragments per kilobase of exon model per million mapped reads). A total of 7252 differentially expressed genes (DEGs) were found in the three NILs after F. graminearum inoculation. As many as 2499 DEGs were detected between NIL1 and NIL3 at 0 hpi, of which 884 DEGs were more abundant in NIL1 and enriched in defense responses. After F. graminearum inoculation, 1070 and 751 genes were exclusively up- and downregulated, respectively, in NIL1 as compared to NIL3. The 1070 upregulated DEGs were enriched in growth/development, photosynthesis/biogenesis, and defense-related responses. Genes encoding putative auxin-induced proteins and GH3 family proteins in auxin signaling pathway were highly induced and lasted longer in NIL3. Genes involved in polar auxin transport (PAT) were more abundant in NIL3 as compared with NIL2.ConclusionsThe qRfg1 confers its resistance to Gibberella stalk rot through both constitutive and induced high expression of defense-related genes; while qRfg2 enhances maize resistance to the disease via relatively lower induction of auxin signaling and repression of PAT. The defense-related transcriptional changes underlying each QTL will undoubtedly facilitate our understanding of the resistance mechanism and resistance breeding for maize stalk rot.

Dataset Information

Effects of a Fusarium Toxin-Contaminated Maize Treated with Sodium Sulfite on Male Piglets in the Presence of an LPS-Induced Acute Inflammation.

Publications

Effects of a <i>Fusarium</i> Toxin-Contaminated Maize Treated with Sodium Sulfite on Male Piglets in the Presence of an LPS-Induced Acute Inflammation.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets