Progress in Mycotoxins Affecting Intestinal Mucosal Barrier Function

Ren, Zhihua; Guo, Chaoyue; Yu, Shumin; Zhu, Ling; Wang, Ya; Hu, Hui; Deng, Junliang

doi:10.3390/ijms20112777

Cited by 84 publications

(72 citation statements)

References 72 publications

(55 reference statements)

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“…The gut barrier plays a crucial role for endotoxin translocation. Different stressors can lead to a comprised gut barrier; that is, suboptimal diet composition [ 33 ], mycotoxins [ 34 , 35 ], heat stress [ 36 ], and weaning stress in pigs [ 37 ] and cattle [ 38 ]. It also needs to be considered that systemic LPS itself (e.g., resulting from any systemic Gram-negative infection) can impact the gut barrier owing to the stimulation and release of cytokines (e.g., TNF), leading to a vicious circle [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Endotoxin Translocation and Gut Inflammation Are Increased in Broiler Chickens Receiving an Oral Lipopolysaccharide (LPS) Bolus during Heat Stress

Reisinger¹,

Emsenhuber²,

Doupovec³

et al. 2020

Toxins

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Lipopolysaccharides (LPS), also termed endotoxins, are the major component of the outer membrane of Gram-negative bacteria. In general, endotoxins in the intestine are considered harmless in healthy animals. However, different stressors, such as heat stress, can lead to a compromised gut barrier, resulting in endotoxin translocation. Chickens are considered to be less sensitive to the effects of LPS compared with other species, for example, humans, pigs, or calves, probably because of the lack of the functional-specific TRAM-TRIF signalling pathway (MyD88-independent). Therefore, six LPS preparations (three different strains with two different preparation methods each) were compared in murine macrophages and characterized according to their MyD88-dependent pathway activation. All tested LPS preparations induced a strong inflammatory response after 4 and 24 h on a murine macrophage cell line. However, there was a similar strong response in the gene expression profile as well as production of nitrite oxide and TNF-alpha from LPS of different strains and preparation methods. On the basis of the results of the in vitro study, one LPS preparation was chosen for the subsequent in vivo study with broilers to assess the effect of an oral LPS bolus (E. coli O55:B5 phenol extracted; 2 mg/kg b.w.) during heat stress conditions (10 h, 36 °C). The most pronounced effects were seen in broilers receiving the oral LPS bolus during heat stress conditions. The endotoxin activity in the intestine as well as the serum concentration of the 3-OH C14 (part of LPS) were increased. In addition, an increased expression of genes related to inflammation and stress response (e.g., IL-6, IL-1beta, HSP70) was observed, whereas the expression of genes associated with gut health (e.g., MUC2, FABP2) was decreased. To conclude, an increase of intestinal LPS combined with heat stress can pose a risk to animal health.

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Section: Discussionmentioning

confidence: 99%

Endotoxin Translocation and Gut Inflammation Are Increased in Broiler Chickens Receiving an Oral Lipopolysaccharide (LPS) Bolus during Heat Stress

Reisinger¹,

Emsenhuber²,

Doupovec³

et al. 2020

Toxins

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“…However, many factors such as stress, infection, and toxins, can lead to gut damage and barrier dysfunction, which can escalate to intestinal diseases such as inflammatory bowel diseases and necrotizing enterocolitis . Deoxynivalenol (DON) is a mycotoxin that commonly contaminates food or feed . Ingestion of DON‐contaminated food or feed leads to altered intestinal structure, compromised intestinal epithelial barrier function, and lower nutrient absorption, which can lead to severe bowel disease .…”

Section: Introductionmentioning

confidence: 99%

“…Deoxynivalenol (DON) is a mycotoxin that commonly contaminates food or feed . Ingestion of DON‐contaminated food or feed leads to altered intestinal structure, compromised intestinal epithelial barrier function, and lower nutrient absorption, which can lead to severe bowel disease . Therefore, effective nutritional approaches are urgently needed to maintain intestinal health after intake of food contaminants.…”

Section: Introductionmentioning

confidence: 99%

EPA and DHA attenuate deoxynivalenol‐induced intestinal porcine epithelial cell injury and protect barrier function integrity by inhibiting necroptosis signaling pathway

et al. 2019

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Abbreviations: DON, deoxynivalenol; Drp1, dynamin-related protein 1; FD4, fluorescein isothiocyanate (FITC)-labeled dextran; HMGB1, high mobility group box-1 protein; IPEC-1, intestinal porcine epithelial cell line 1; LDH, lactate dehydrogenase; MLKL, mixed lineage kinase-like protein; PGAM5, phosphoglycerate mutase family 5; RIP1, receptor interacting protein kinase 1; RIPK3, receptor interacting protein kinase 3; TEER, transepithelial electrical resistance; TNFR1, tumor necrosis factor receptor 1. Abstract Deoxynivalenol (DON) is one of the most common mycotoxins that contaminates food or feed and cause intestinal damage. Long-chain n-3 polyunsaturated fatty acids (PUFA) such as EPA and DHA exert beneficial effects on intestinal integrity in animal models and clinical trials. Necroptosis signaling pathway plays a critical role in intestinal cell injury. This study tested the hypothesis that EPA and DHA could alleviate DON-induced injury to intestinal porcine epithelial cells through modulation of the necroptosis signaling pathway. Intestinal porcine epithelial cell 1 (IPEC-1) cells were cultured with or without EPA or DHA (6.25-25 μg/mL) in the presence or absence of 0.5 μg/mL DON for indicated time points. Cell viability, cell number, lactate dehydrogenase (LDH) activity, cell necrosis, transepithelial electrical resistance (TEER), fluorescein isothiocyanate-labeled dextran 4kDa (FD4) flux, tight junction protein distribution, and protein abundance of necroptosis related signals were determined. EPA and DHA promoted cell growth indicated by higher cell viability and cell number, and inhibited cell injury indicated by lower LDH activity in the media. EPA and DHA also improved intestinal barrier function, indicated by higher TEER and lower permeability of FD4 flux as well as increased proportions of tight junction proteins located in the plasma membrane. Moreover, EPA and DHA decreased cell necrosis demonstrated by live cell imaging and transmission electron microscopy. Finally, EPA and DHA downregulated protein expressions of necroptosis related signals including tumor necrosis factor receptor (TNFR1), receptor interacting protein kinase 1 (RIP1), RIP3, phosphorylated mixed lineage kinase-like protein (MLKL), phosphoglycerate mutase family 5 (PGAM5), dynamin-related protein 1 (Drp1), and high mobility group box-1 protein (HMGB1). EPA and DHA also inhibited protein expression of caspase-3 and caspase-8. These results suggest that EPA and DHA 2484 | XIAO et Al.

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“…The increase in serum LPS content in the HFD+CSP group may be due to the transfer of harmful bacteria from the colon to the small intestine, resulting in the excessive proliferation of physical barrier cells in the small intestine and the absorption of LPS and chylomicrons (CMs) by the small intestinal epithelial cells [57,58]. In addition to the intestinal physical barrier, the intestinal tract also includes an immune barrier, a chemical barrier and a biological barrier, which are associated with the composition of microorganisms in the intestinal tract [59,60]. Damage to the biological barrier in the colon can also cause a bacterial product shift.…”

Section: Plos Onementioning

confidence: 99%

Polysaccharides isolated from Cordyceps Sinensis contribute to the progression of NASH by modifying the gut microbiota in mice fed a high-fat diet

et al. 2020

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Various dietary fibers are considered to prevent obesity by modulating the gut microbiota. Cordyceps sinensis polysaccharide (CSP) is a soluble dietary fiber known to have protective effects against obesity and related diseases, but whether these effects induce any side effects remains unknown. The function and safety of CSP were tested in high-fat diet (HFD)-feding C57BL/6J mice. The results revealed that even though CSP supplementation could prevent an increase in body weight, it aggravated liver fibrosis and steatosis as evidenced by increased inflammation, lipid metabolism markers, insulin resistance (IR) and alanine aminotransferase (ALT) in HFD-induced obesity. 16S rDNA gene sequencing was used to analyze the gut microbiota composition, and the relative abundance of the Actinobacteria phylum, including the Olsenella genus, was significantly higher in CSP-treated mice than in HFD-fed mice. CSP supplementation may increase the proportion of Actinobacteria, which can degrade CSP. The high level of Actinobacteria aggravated the disorder of the intestinal flora and contributed to the progression from obesity to nonalcoholic steatohepatitis (NASH) and related diseases.

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Progress in Mycotoxins Affecting Intestinal Mucosal Barrier Function

Cited by 84 publications

References 72 publications

Endotoxin Translocation and Gut Inflammation Are Increased in Broiler Chickens Receiving an Oral Lipopolysaccharide (LPS) Bolus during Heat Stress

Endotoxin Translocation and Gut Inflammation Are Increased in Broiler Chickens Receiving an Oral Lipopolysaccharide (LPS) Bolus during Heat Stress

EPA and DHA attenuate deoxynivalenol‐induced intestinal porcine epithelial cell injury and protect barrier function integrity by inhibiting necroptosis signaling pathway

Polysaccharides isolated from Cordyceps Sinensis contribute to the progression of NASH by modifying the gut microbiota in mice fed a high-fat diet

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