Selenium maintains intestinal epithelial cells to activate M2 macrophages against deoxynivalenol injury.

Selenium (Se) is indispensable in alleviating various types of intestinal injuries. Here, we thoroughly investigated the protective effect of Se on the regulation of the epithelial cell-M2 macrophages pathway in deoxynivalenol (DON)-induced intestinal damage. In the present study, Se has positive impacts on gut health by improving gut barrier function and reducing the levels of serum DON in vivo. Furthermore, our study revealed that Se supplementation increased the abundances of GPX4, p-PI3K, and AKT, decreased the levels of 4-HNE and inhibited ferroptosis. Moreover, when mice were treated with DON and Fer-1(ferroptosis inhibitor), ferroptosis was suppressed and PI3K/AKT pathway was activated. These results indicated that GPX4-PI3K/AKT-ferroptosis was a predominant pathway in DON-induced intestinal inflammation. Interestingly, we discovered that both the number of M2 anti-inflammatory macrophages and the levels of CSF-1 decreased while the pro-inflammatory cytokine IL-6 increased in the intestine and MODE-K cells supernatant. Therefore, Se supplementation activated the CSF-1-M2 macrophages axis, resulting in a decrease in IL-6 expression and an enhancement of the intestinal anti-inflammatory capacity. This study provides novel insights into how intestinal epithelial cells regulate the CSF-1-M2 macrophage pathway, which is essential in maintaining intestinal homeostasis confer to environmental hazardous stimuli.

Overview of T-2 Toxin Enterotoxicity: From Toxic Mechanisms and Detoxification to Future Perspectives.

Fusarium species produce a secondary metabolite known as T-2 toxin, which is the primary and most harmful toxin found in type A trichothecenes. T-2 toxin is widely found in food and grain-based animal feed and endangers the health of both humans and animals. T-2 toxin exposure in humans and animals occurs primarily through food administration; therefore, the first organ that T-2 toxin targets is the gut. In this overview, the research progress, toxicity mechanism, and detoxification of the toxin T-2 were reviewed, and future research directions were proposed. T-2 toxin damages the intestinal mucosa and destroys intestinal structure and intestinal barrier function; furthermore, T-2 toxin disrupts the intestinal microbiota, causes intestinal flora disorders, affects normal intestinal metabolic function, and kills intestinal epidermal cells by inducing oxidative stress, inflammatory responses, and apoptosis. The primary harmful mechanism of T-2 toxin in the intestine is oxidative stress. Currently, selenium and plant extracts are mainly used to exert antioxidant effects to alleviate the enterotoxicity of T-2 toxin. In future studies, the use of genomic techniques to find upstream signaling molecules associated with T-2 enterotoxin toxicity will provide new ideas for the prevention of this toxicity. The purpose of this paper is to review the progress of research on the intestinal toxicity of T-2 toxin and propose new research directions for the prevention and treatment of T-2 toxin toxicity.

Sodium butyrate alleviates deoxynivalenol-induced porcine intestinal barrier disruption by promoting mitochondrial homeostasis via PCK2 signaling.

Deoxynivalenol (DON) is one of the most plentiful trichothecenes occurring in food and feed, which brings severe health hazards to both animals and humans. This study aims to investigate whether sodium butyrate (NaB) can protect the porcine intestinal barrier from DON exposure through promoting mitochondrial homeostasis. In a 4-week feeding experiment, 28 male piglets were allocated according to a 2 by 2 factorial arrangement of treatments with the main factors including supplementation of DON (< 0.8 vs. 4.0 mg/kg) and NaB (0.0 vs. 2 g/kg) in a corn/soybean-based diet. Dietary NaB supplementation mitigated the damaged mitochondrial morphology within the jejunal mucosa and the disrupted gut epithelial tight junctions irritated by DON. In IPEC-J2 cells, we found efficient recovery of the intestinal epithelial barrier occurred following NaB administration. This intestinal barrier reparation was facilitated by NaB-induced PCK2-mediated glyceroneogenesis and restoration of mitochondrial structure and function. In conclusion, we elucidated a mechanism of PCK2-mediated improvement of mitochondrial function by NaB to repair porcine intestinal barrier disruption during chronic DON exposure. Our findings highlight the promise of NaB for use in protecting against DON-induced gut epithelial tight junction disruption in piglets.

Effect of Lactobacillus sp. and yeast supplementation on performance and some blood attributes in deoxynivalenol-challenged broiler chickens.

An experiment was conducted to evaluate the effect of different concentrations of probiotic (Lactobacillus sp.) and yeast (Saccharomycese cerevisiae) on performance, organ attributes and blood traits in broiler chickens. A total of 360 one-day-old female broiler chickens (Hubbard)® were allocated to 9 treatments and four replicates (10 birds per replication). The trail was performed in a completely randomized design (3 × 3 factorial arrangement) to examine the interaction effect of three concentrations of Lactobacillus sp. (0, 0.2 and 0.4 g/kg) and yeast (0, 0.75 and 1.5 g/kg) in deoxynivalenol (DON)-contaminated diets. The results showed that consumption of Lactobacillus sp. and yeast in DON-contaminated diets did not have a significant effect on broiler performance except for feed intake during starter period which was enhanced by yeast administration (P < 0.05). Increasing the Lactobacillus sp. content also reduced (P = 0.05) the proportional liver weight. Administration of Lactobacillus sp. to DON diets increased total protein, albumin and globulin concentrations (P < 0.05). Calcium and creatinine were influenced by yeast and Lactobacillus sp., respectively. Yeast (1.5 g/kg) and Lactobacillus sp. (0.2 g/kg) and combination of two additives (1.5 × 0.2) led to lower triglyceride concentration compared to DON group (P < 0.05). The DON diet increased aspartate amino transferase (AST) and lactate dehydrogenase (LDH) enzymes concentrations; while, inclusion of 0.4 g/kg Lactobacillus sp. to DON diet decreased AST and LDH enzymes concentrations (P < 0.05). In conclusion, administration of Lactobacillus sp. and yeast could not influence the performance of DON-fed birds; but these additives could reduce negative effects of DON on enzyme activities and some blood attributes.

Microcapsules loaded with date seed extract and its inhibitory potential to modulate the toxic effects of mycotoxins in mice received mold-contaminated diet.

Mycotoxins are the secondary fungal metabolites generally produced by wide range of fungi including aflatoxins (AF), ochratoxin A (OTA), fumonisins (FB), zearalenone (ZEN), and deoxynivalenol (DON). Nowadays, they are main concern to food and agricultural commodities due to undesirable health and socio-economic effect. This investigation was designed to synthesized microcapsules loaded the bioactive compounds of date seed and evaluated its inhibitory activities in mice received mold-contaminated diet. The finding revealed that the developed microcapsule is homogenous and mostly spherical with size of 2.58 µm with acceptable PDI of 0.21. The main phytochemical has been confirmed by HPLC analysis were xylose, fructose, mannose, glucose, and galactose with the respective values of 41.95%, 2.24%, 5.27%, and 0.169%. The in vivo analyses manifested that the mice received date seed microcapsules significantly (p < 0.05) improved the average daily weight gain, feed intake, liver enzymes (ALT, ALP, and AST), and lipid peroxidation values compare to mice group received mycotoxin-contaminated diet. Furthermore, encapsulation date seed bioactive compounds notably up-regulated the expression of GPx, SOD, IFN-γ, and IL-2 genes while down-regulated the iNOS gene. Consequently, the novel microcapsules loaded date seed is suggested to be considered as a promising mycotoxin inhibitor.

[Single-laboratory Validation of an Analytical Method for Detarmination of Fusarium toxins in Buckwheat and Job's Tears].

Fusarium species infect the major cereals consumed as food and feed, contaminating them with various toxic secondary metabolites known as toxins. Among these toxins, which include trichothecenes, zearalenone (ZEA), and fumonisins, the type-B trichothecene deoxynivalenol (DON) is generally considered as the most important. The present study evaluates an analytical method for the detection and quantification of multiple Fusarium toxins, namely, DON, acetyl forms of DON (3-Ac-DON and 15-Ac-DON), a glycoside form of DON (DON-3G), and other Fusarium toxins (nivalenol, an acetyl form of NIV (fusarenonX), T-2 and HT-2 toxins, diacetoxyscirpenol, and ZEA) in Job's tears and buckwheat.

Metaproteomics Reveals Alteration of the Gut Microbiome in Weaned Piglets Due to the Ingestion of the Mycotoxins Deoxynivalenol and Zearalenone.

The ingestion of mycotoxins can cause adverse health effects and represents a severe health risk to humans and livestock. Even though several acute and chronic effects have been described, the effect on the gut metaproteome is scarcely known. For that reason, we used metaproteomics to evaluate the effect of the mycotoxins deoxynivalenol (DON) and zearalenone (ZEN) on the gut microbiome of 15 weaned piglets. Animals were fed for 28 days with feed contaminated with different concentrations of DON (DONlow: 870 µg DON/kg feed, DONhigh: 2493 µg DON/kg feed) or ZEN (ZENlow: 679 µg ZEN/kg feed, ZENhigh: 1623 µg ZEN/kg feed). Animals in the control group received uncontaminated feed. The gut metaproteome composition in the high toxin groups shifted compared to the control and low mycotoxin groups, and it was also more similar among high toxin groups. These changes were accompanied by the increase in peptides belonging to Actinobacteria and a decrease in peptides belonging to Firmicutes. Additionally, DONhigh and ZENhigh increased the abundance of proteins associated with the ribosomes and pentose-phosphate pathways, while decreasing glycolysis and other carbohydrate metabolism pathways. Moreover, DONhigh and ZENhigh increased the abundance of the antioxidant enzyme thioredoxin-dependent peroxiredoxin. In summary, the ingestion of DON and ZEN altered the abundance of different proteins associated with microbial metabolism, genetic processing, and oxidative stress response, triggering a disruption in the gut microbiome structure.

Phytobiotics with Adsorbent to Mitigate Toxicity of Multiple Mycotoxins on Health and Growth of Pigs.

Phytobiotics with a mycotoxin adsorbent were used to mitigate negative effects of multiple mycotoxins in diets fed to pigs. In experiment 1, 120 pigs (11.6 kg body weight; BW) were assigned to five treatments (three pigs/pen) and fed for 28 days. Treatments were CON (control), MTD (CON + 2.5 mg/kg of deoxynivalenol), DP (MTD + phytobiotics at 0.1%), and DPA1 and DPA2 (MTD + phytobiotics and adsorbent at 0.1% and 0.2%, respectively). In experiment 2, 96 pigs (28.5 kg BW) were assigned to four treatments (three pigs/pen) and fed for 26 days. Treatments were CON, MTAF (CON + 0.19 mg/kg of aflatoxin and 8 mg/kg of fumonisins), AFP (MTAF + phytobiotics at 0.1%), and AFPA (MTAF + phytobiotics and adsorbent at 0.1%). Growth performance was measured weekly, and blood was sampled at the end of study to measure hepatic function and inflammatory status (TNF-α). Data were analyzed using the MIXED procedure. In experiment 1, pigs fed MTD, DP, DPA1, and DPA2 had smaller (p < 0.05) BW than CON. Pigs fed DPA2 had greater (p < 0.05) BW than MTD. Pigs fed DP and DPA2 tended to have lower (p < 0.1) serum total protein than CON. Pigs fed MTD and DPA2 tended to have higher (p < 0.1) alanine aminotransferase than CON. Similarly, pigs fed MTD, DP, and DPA2 tended to have higher (p < 0.1) urea nitrogen/creatinine than CON. In experiment 2, pigs fed MTAF, AFP, and AFPA had smaller (p < 0.05) BW than CON. Pigs fed MTAF, AFP, and AFPA had smaller (p < 0.05) ADFI than CON. Pigs fed AFPA had higher (p < 0.05) aspartate aminotransferase than CON and MTAF. Pigs fed AFP and AFPA had higher (p < 0.05) alanine aminotransferase than CON. Pigs fed MTAF, AFP, and AFPA had lower (p < 0.05) urea nitrogen/creatinine than CON. Pigs fed AFPA had higher (p < 0.05) TNF-α than CON and MTAF. In conclusion, feeding an additional 2.5 mg/kg of deoxynivalenol or 0.19 mg/kg of aflatoxin with 8 mg/kg of fumonisins reduced the growth of pigs. Deoxynivalenol compromised the hepatic function of pigs. Phytobiotics with adsorbent could partly overcome the detrimental effects of mycotoxins.

Mitigation Effects of Bentonite and Yeast Cell Wall Binders on AFB1, DON, and OTA Induced Changes in Laying Hen Performance, Egg Quality, and Health.

The objective of this study was to evaluate the efficacy of mycotoxin binders in reducing the adverse effects of co-occurring dietary aflatoxin B1 (AFB1), deoxynivalenol (DON) and ochratoxin A (OTA) on laying hens. Three hundred and sixty 26-week-old Roman laying hens were randomly allocated into four experimental groups with 10 replicates of nine birds each. The four groups received either a basal diet (BD; Control), a BD supplemented with 0.15 mg/kg AFB1 + 1.5 mg/kg DON + 0.12 mg/kg OTA (Toxins), a BD + Toxins with Toxo-HP binder (Toxins + HP), or a BD + Toxins with TOXO XL binder (Toxins + XL) for 12 weeks. Compared to the control, dietary supplementation of mycotoxins decreased (P < 0.10) total feed intake, total egg weight, and egg-laying rate, but increased feed/egg ratio by 2.5-6.1% and mortality during various experimental periods. These alterations induced by mycotoxins were alleviated by supplementation with both TOXO HP and XL binders (P < 0.10). Furthermore, dietary mycotoxins reduced (P < 0.05) eggshell strength by 12.3% and caused an accumulation of 249 µg/kg of DON in eggs at week 12, while dietary supplementation with TOXO HP or XL mitigated DON-induced changes on eggshell strength and prevented accumulation of DON in eggs (P < 0.05). Moreover, dietary mycotoxins increased relative liver weight, but decreased spleen and proventriculus relative weights by 11.6-22.4% (P < 0.05). Mycotoxin exposure also increased alanine aminotransferase activity and reduced immunoglobulin (Ig) A, IgM, and IgG concentrations in serum by 9.2-26.1% (P < 0.05). Additionally, mycotoxin exposure induced histopathological damage and reduced villus height, villus height/crypt depth, and crypt depth in duodenum, jejunum and (or) ileum (P < 0.05). Notably, most of these histological changes were mitigated by supplementation with both TOXO HP and XL (P < 0.05). In conclusion, the present study demonstrated that the mycotoxin binders TOXO HP and XL can help to mitigate the combined effects of AFB1, DON, and OTA on laying hen performance, egg quality, and health.

Impaired Performance of Broiler Chickens Fed Diets Naturally Contaminated with Moderate Levels of Deoxynivalenol.

Mycotoxin exposure is common in the poultry industry. Deoxynivalenol (DON) is usually detected at levels below the maximum threshold (5000 ppb), but depending on diet and age, broiler performance can be affected. We evaluated the effects of 900 ppb and 2300 ppb DON on the performance, intestinal morphometry, and lesion scores of broiler chickens. One-day-old male Ross broilers (n = 736) were divided into 4 treatments with 8 replicates each, and a pen containing 23 birds was the experimental unit. The animals were fed diets naturally contaminated with two levels of DON: 900 (Low DON-LD) or 2300 (Moderate DON-MD) ppb, with or without activated charcoal, over 28 days. After this, all birds were fed a marginally DON-contaminated diet without charcoal. During the first 28 days, body weight gain (BWG) and feed conversion ratio (FCR) were significantly impaired when broilers were fed a MD diet without activated charcoal. Even after feeding a marginally contaminated diet from D28-35, birds previously fed the MD diet presented a significantly lower performance. The villus height:crypt depth (VH:CD) ratio was significantly higher in the ileum from 14-day-old broilers fed the MD when compared with the LD diet. At D28, the MD diet caused decreased villus height (VH) and increased crypt depth (CD), affecting VH:CD ratio in both intestinal segments, with higher levels in the jejunum from 28-day-old broilers fed a non-supplemented LD diet. Broiler production was negatively affected by DON, even at moderate levels (2300 ppb).

Mycotoxin Occurrence, Toxicity, and Detoxifying Agents in Pig Production with an Emphasis on Deoxynivalenol.

This review aimed to investigate the occurrence of mycotoxins, their toxic effects, and the detoxifying agents discussed in scientific publications that are related to pig production. Mycotoxins that are of major interest are aflatoxins and Fusarium toxins, such as deoxynivalenol and fumonisins, because of their elevated frequency at a global scale and high occurrence in corn, which is the main feedstuff in pig diets. The toxic effects of aflatoxins, deoxynivalenol, and fumonisins include immune modulation, disruption of intestinal barrier function, and cytotoxicity leading to cell death, which all result in impaired pig performance. Feed additives, such as mycotoxin-detoxifying agents, that are currently available often combine organic and inorganic sources to enhance their adsorbability, immune stimulation, or ability to render mycotoxins less toxic. In summary, mycotoxins present challenges to pig production globally because of their increasing occurrences in recent years and their toxic effects impairing the health and growth of pigs. Effective mycotoxin-detoxifying agents must be used to boost pig health and performance and to improve the sustainable use of crops.

The Effects of Selenium on Wheat Fusarium Head Blight and DON Accumulation Were Selenium Compound-Dependent.

Fusarium head blight (FHB) caused by Fusarium graminearum not only results in severe yield losses, but also contaminates wheat grains with deoxynivalenol (DON) toxins. Prevention and control of FHB and DON contamination rely mainly on resistant varieties and fungicides. Selenium (Se) is an essential element for humans and animals, and also a beneficial element for plants. In this work, four Se compounds, i.e., sodium selenite (Na2SeO3), sodium selenate (Na2SeO4), selenomethionine (SeMet) and selenocysteine (SeCys2), were supplemented in a trichothecene biosynthesis induction (TBI) solid medium at different dosages in in vitro experiments. The four Se compounds at the dosage of 20 mg∙L-1 were sprayed onto wheat spikes immediately after inoculation at anthesis. All four of the Se compounds significantly inhibited the mycelial growth and DON production in the in vitro experiment; however, in planta, their effects on FHB severity and toxin accumulation in grains were compound-dependent. SeMet consistently negatively regulated fungal growth and DON accumulation both in vitro and in planta, which could be a novel and proconsumer strategy for reducing the detriment of wheat FHB disease and DON accumulation.

Anorexic action of fusarenon-x in the hypothalamus and intestine.

There is a lack of information available on the anorexic action of fusarenon-x (FX), which is a sesquiterpenoid mycotoxin. In this study, we investigated the changes in the hypothalamus and small intestine related to appetite after oral FX exposure. The time-course change of food intake after oral FX exposure (0.5, 1.0, and 2.5 mg/kg bw) in B6C3F1 mice showed that 2.5 mg/kg bw of FX significantly suppressed food intake during 3-6 h compared to the control. Furthermore, the total food intake for 24 h was lower in the group exposed to FX than in the control. The FX exposure (2.5 mg/kg bw for 3 h) significantly increased mRNA levels of anorexic hormones (pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcription (CART)) without changing the mRNA levels of orexigenic hormones. In addition, FX exposure indicated significantly higher mRNA levels of possible downstream targets of anorexic POMC neurons, such as the melanocortin 4 receptor (MC4R), brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor B (TrkB), in the hypothalamus compared to the control. FX exposure also significantly increased the mRNA level of inflammatory cytokines (tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß)) and activated nuclear factor-kappa B (NF-κB), which is a regulatory factor for POMC in the hypothalamus. In the intestine, FX exposure did not affect the mRNA level of anorexic peptide YY but significantly elevated that of anorexic cholecystokinin (CCK) and regulatory factors for CCK (calcium-sensing receptor (CaSR), the transient receptor potential ankyrin-1 channel (TRPA1), and transient receptor potential cation channel subfamily M member 5 (TRPM5)). These results suggest that FX sequentially induces inflammatory cytokine expression, NF-κB activation, and POMC expression in the hypothalamus. FX also induces CCK expression in the intestine possibly via induction of CaSR, TRPM5, and TRPA1 expression. These changes will eventually lead to the anorexic action of FX.

Zearalenone and Metabolites in Livers of Turkey Poults and Broiler Chickens Fed with Diets Containing Fusariotoxins.

Zearalenone (ZEN) and metabolites were measured in livers of turkeys and broilers fed a control diet free of mycotoxins, a diet that contained 0.5 mg/kg ZEN (ZEN diet), and a diet that contained 0.5, 5, and 20 mg/kg of ZEN, fumonisins, and deoxynivalenol, respectively (ZENDONFB diet). The feed was individually distributed to male Grade Maker turkeys from the 55th to the 70th day of age and to male Ross chickens from the 1st to the 35th day of age, without any signs of toxicity. Together, the free and conjugated forms of ZEN, α- and ß-zearalenols (ZOLs), zearalanone (ZAN), and α- and ß-zearalanols (ZALs) were measured by UHPLC-MS/MS with [13C18]-ZEN as an internal standard and immunoaffinity clean-up of samples. ZAN and ZALs were not detected. ZEN and ZOLs were mainly found in their conjugated forms. α-ZOL was the most abundant and was found at a mean concentration of 2.23 and 1.56 ng/g in turkeys and chickens, respectively. Consuming the ZENDONFB diet significantly increased the level of total metabolites in the livers of chickens. Furthermore, this increase was more pronounced for the free forms of α-ZOL than for the conjugated forms. An investigation of the presence of ZEN and metabolites in muscle with the methods validated for the liver failed to reveal any traces of these contaminants in this tissue. These results suggest that concomitant dietary exposure to deoxynivalenol (DON) and fumonisins (FB) may alter the metabolism and persistence of ZEN and its metabolites in the liver.

Investigation of the Efficacy of a Postbiotic Yeast Cell Wall-Based Blend on Newly-Weaned Pigs under a Dietary Challenge of Multiple Mycotoxins with Emphasis on Deoxynivalenol.

Pigs are highly susceptible to mycotoxins. This study investigated the effects of a postbiotic yeast cell wall-based blend (PYCW; Nicholasville, KY, USA) on growth and health of newly-weaned pigs under dietary challenge of multiple mycotoxins. Forty-eight newly-weaned pigs (21 d old) were individually allotted to four dietary treatments, based on a three phase-feeding, in a randomized complete block design (sex; initial BW) with two factors for 36 d. Two factors were dietary mycotoxins (deoxynivalenol: 2000 µg/kg supplemented in three phases; and aflatoxin: 200 µg/kg supplemented only in phase 3) and PYCW (0.2%). Growth performance (weekly), blood serum (d 34), and jejunal mucosa immune and oxidative stress markers (d 36) data were analyzed using MIXED procedure of SAS. Mycotoxins reduced (p < 0.05) average daily feed intake (ADFI) and average daily gain (ADG) during the entire period whereas PYCW did not affect growth performance. Mycotoxins reduced (p < 0.05) serum protein, albumin, creatinine, and alanine aminotransferase whereas PYCW decreased (p < 0.05) serum creatine phosphokinase. Neither mycotoxins nor PYCW affected pro-inflammatory cytokines and oxidative damage markers in the jejunal mucosa. No interaction was observed indicating that PYCW improved hepatic enzymes regardless of mycotoxin challenge. In conclusion, deoxynivalenol (2000 µg/kg, for 7 to 25 kg body weight) and aflatoxin B1 (200 µg/kg, for 16 to 25 kg body weight) impaired growth performance and nutrient digestibility of newly-weaned pigs, whereas PYCW could partially improve health of pigs regardless of mycotoxin challenge.

Maternal Supplementation of Food Ingredient (Prebiotic) or Food Contaminant (Mycotoxin) Influences Mucosal Immune System in Piglets.

The early life period is crucial for the maturation of the intestinal barrier, its immune system, and a life-long beneficial host-microbiota interaction. The study aims to assess the impact of a beneficial dietary (short-chain fructooligosaccharides, scFOS) supplementation vs. a detrimental dietary environment (such as mycotoxin deoxynivalenol, DON) on offspring intestinal immune system developmental profiles. Sows were given scFOS-supplemented or DON-contaminated diets during the last 4 weeks of gestation, whereas force-feeding piglets with DON was performed during the first week of offspring life. Intestinal antigen-presenting cell (APC) subset frequency was analyzed by flow cytometry in the Peyer's patches and in lamina propria and the responsiveness of intestinal explants to toll-like receptor (TLR) ligands was performed using ELISA and qRT-PCR from post-natal day (PND) 10 until PND90. Perinatal exposure with scFOS did not affect the ontogenesis of APC. While it early induced inflammatory responses in piglets, scFOS further promoted the T regulatory response after TLR activation. Sow and piglet DON contamination decreased CD16+ MHCII+ APC at PND10 in lamina propria associated with IFNγ inflammation and impairment of Treg response. Our study demonstrated that maternal prebiotic supplementation and mycotoxin contamination can modulate the mucosal immune system responsiveness of offspring through different pathways.

Efficacy of Mycotoxin Detoxifiers on Health and Growth of Newly-Weaned Pigs under Chronic Dietary Challenge of Deoxynivalenol.

The efficacy of yeast-based mycotoxin detoxifiers on health and growth performance of newly-weaned pigs (27-d-old) fed diets naturally contaminated with deoxynivalenol was investigated. Sixty pigs were individually assigned to five treatments for 34 d: NC (negative control, 1.2 mg/kg of deoxynivalenol); PC (positive control, 3.2 mg/kg of deoxynivalenol); CYC (PC + clay/yeast culture-based product, 0.2%); CYE (PC + clay/yeast cell wall/plant extracts/antioxidants-based product, 0.2%); and CYB (PC + clay/inactivated yeast/botanicals/antioxidants-based product, 0.2%). Blood and jejunal mucosa were sampled, and data were analyzed using Proc Mixed of SAS with pre-planned contrasts. Deoxynivalenol reduced the average daily gain (ADG) in phase 3. Pigs fed CYC had greater overall ADG, average daily feed intake during phase 3, and gain to feed ratio during phase 2 than PC. At d 14, deoxynivalenol reduced blood urea nitrogen/creatinine and tended to reduce blood urea nitrogen. Pigs fed CYB tended to have greater aspartate aminotransferase than PC. At d 34, pigs fed CYC and CYB tended to have lower serum creatine phosphokinase than PC. Pigs fed CYE had lower blood urea nitrogen/creatinine than PC. In jejunal mucosa, deoxynivalenol tended to increase malondialdehydes and decrease glutathione. Pigs fed CYE and CYB had lower malondialdehydes, pigs fed CYB had greater glutathione and tended to have lower immunoglobulin A than PC. Pigs fed CYC and CYE tended to have lower interleukin 8 than PC. In summary, deoxynivalenol challenge (1.2 vs. 3.2 mg/kg) mildly compromised growth performance and increased the oxidative stress of pigs. Mycotoxin detoxifiers could partially overcome deoxynivalenol toxicity enhancing liver health, whereas CYE and CYB reduced oxidative stress, and CYC and CYB reduced immune activation. In conclusion, yeast-based detoxifiers with functional components as clay/inactivated yeast/botanicals/antioxidants had increased detoxifying properties in newly-weaned pigs challenged with deoxynivalenol, potentially by enhancing adsorbability, immune function, gut health, and reducing oxidative stress.

Sodium Butyrate Protects the Intestinal Barrier by Modulating Intestinal Host Defense Peptide Expression and Gut Microbiota after a Challenge with Deoxynivalenol in Weaned Piglets.

This study aims to determine whether sodium butyrate (SB) could antagonize deoxynivalenol (DON)-induced intestinal epithelial dysfunction. In a four-week feeding trial, twenty-eight barrows were randomly divided into four treatments: (1) uncontaminated basal diet (control); (2) 4 mg/kg DON-contaminated diet (DON); (3) basal diet supplemented with 0.2% SB (SB); and (4) 4 mg/kg DON + 0.2% SB (DON + SB). A decrease in performance was observed in DON-exposed animals, which was prevented by the dietary SB supplementation. DON exposure also depressed the expression of host defense peptides (HDPs) in the intestine, impaired the intestinal barrier integrity, and disturbed the gut microbiota homeostasis. These alterations induced by DON were attenuated by SB supplementation. The supplementation of 0.2% SB ameliorated the adverse effects of DON on the liver in terms of hepatic lesions as well as serum concentrations of alkaline phosphatase and aspartate aminotransferase. In IPEC-J2 cells, pretreatment with SB alleviated the DON-induced decreased cell viability. Additionally, the NOD2/caspase-12 pathway participated in the alleviation of SB on DON-induced diminished HDP expression. Taken together, these data demonstrated that SB protected piglets from DON-induced intestinal barrier dysfunction potentially through stimulation of intestinal HDP assembly and regulation in gut microbiota.

Dietary Baicalin Zinc Supplementation Alleviates Oxidative Stress and Enhances Nutrition Absorption in Deoxynivalenol Challenged Pigs.

BACKGROUND: Deoxynivalenol contamination is increasing worldwide, presenting great challenges to food security and causing great economic losses in the livestock industry. OBJECTIVE: This study was conducted to determine the protective effect of baicalin zinc as a dietary supplement on pigs fed with a deoxynivalenol contaminated diet. METHODS: A total of 40 weaned pigs (21 d of age; 6.13 ± 0.42 kg average BW) were randomly assigned (10 pigs/group) to 4 dietary treatments: basal diet (Con group), basal diet + 4 mg/kg DON (DON group), basal diet + 5 g/kg BZN (BZN group), and basal diet + 5 g/kg BZN + 4 mg/kg DON (DBZN group) for a 14-d period. Seven randomly-selected pigs from each treatment were killed for blood and tissue sampling. RESULTS: The results showed that piglets challenged with DON exhibited significantly reduced levels of ADG, ADFI, and F/G (p < 0.05). BZN supplemented diets significantly suppressed the protein expression of p-Nrf2, p-NF-kB, and HO-1 in the jejunum of DON challenged piglets (p < 0.05). In liver, DON markedly increased the mRNA expression of P70S6K and HSP70 in piglets fed the basal diet, but significantly reduced that of HO-1, NQO-1, NF-kB, AMPKα2 and HSP70 in piglets fed the BZN supplemented diet (p < 0.05). Dietary supplementation with BZN markedly increased the T-AOC level of serum in weaned piglets (p < 0.05). In jejunum, dietary supplementation with BZN activated the mRNA expression of ZIP4 in piglets (p < 0.05), BZN supplementation significantly suppressed the activity of sucrose and increased the protein concentration in chyme (p < 0.05). CONCLUSION: BZN can play a protective role by reducing oxidative stress and enhancing nutrient absorption in pigs fed DON-contaminated diets.

Isolation and Characterization of a Deoxynivalenol-Degrading Bacterium Bacillus licheniformis YB9 with the Capability of Modulating Intestinal Microbial Flora of Mice.

Deoxynivalenol (DON) is one of the most prevalent food- and feed-associated mycotoxins. It frequently contaminates agricultural commodities and poses serious threats to human and animal health and leads to tremendous economic losses globally. Much attention has been paid to using microorganisms to detoxify DON. In this study, a Bacillus licheniformis strain named YB9 with a strong ability to detoxify DON was isolated and characterized from a moldy soil sample. YB9 could degrade more than 82.67% of 1 mg/L DON within 48 h at 37 °C and showed strong survival and DON degradation rate at simulated gastric fluid. The effects of YB9 on mice with DON intragastrical administration were further investigated by biochemical and histopathological examination and the gut microbiota was analyzed by 16S rRNA Illumina sequencing technology. The results showed that DON increased the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatinine (Cr), decreased those of immunoglobulin G (IgG) and IgM in serum, and resulted in severe pathological damage of the liver, kidney, and spleen. By contrast, YB9 supplementation obviously inhibited or attenuated the damages caused by DON in mice. In addition, YB9 addition repaired the DON-induced dysbiosis of intestinal flora, characterized by recovering the balance of Firmicutes and Bacteroidetes to the normal level and decreasing the abundance of the potentially harmful bacterium Turicibacter and the excessive Lactobacillus caused by DON. Taken together, DON-degrading strain YB9 might be used as potential probiotic additive for improving food and feed safety and modulating the intestinal microbial flora of humans and animals.