Effect of Fumonisin B1 on Proliferation and Apoptosis of Intestinal Porcine Epithelial Cells

Wang, Tianjie; Lei, Hongyu; Zhou, Lihua; Tang, Mimi; Liu, Qing; Feng, Lei; Li, Qing; Su, Jianming

doi:10.3390/toxins14070471

Cited by 4 publications

(2 citation statements)

References 33 publications

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“…Previous results showed that FB1 exposure in human gastric epithelial (GES-1), kidney tubular epithelial (HK-2), and monkey kidney (MARC-145) cells caused cytotoxicity and cell death [29][30][31], while FB1 in human liver hepatoblastoma (HepG2) cells led to oxidative stress [32]. FB1 could also induce cytotoxicity proliferation inhibition and promote cell death in IPEC-J2 cells from the porcine intestine [33]. Consistent with these reported results, this study also revealed that FB1 could dose-and time-dependently exert cytotoxicity on IEC-6 cells, causing growth inhibition and MMP loss, promoting LDH release, and enhancing ROS production.…”

Section: Discussionmentioning

confidence: 99%

Longan Polysaccharides with Covalent Selenylation Combat the Fumonisin B1-Induced Cell Toxicity and Barrier Disruption in Intestinal Epithelial (IEC-6) Cells

Yu,

Zhao

2023

Nutrients

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In this study, the soluble, but non-digestible, longan (Dimocarpus longan Lour.) polysaccharides (LP) were extracted from dried longan fruits and then chemically selenylated to produce two selenylated products, namely SeLP1 and SeLP2, with different selenylation extents. The aim was to investigate their protective effects on rat intestinal epithelial (IEC-6) cells exposed to the food toxin fumonisin B1 (FB1). LP only contained total Se content of less than 0.01 g/kg, while SeLP1 and SeLP2 were measured with respective total Se content of up to 1.46 and 4.79 g/kg. The cell viability results showed that these two selenylated products were more efficient than LP in the IEC-6 cells in alleviating FB1-induced cell toxicity, suppressing lactate dehydrogenase (LDH) release, and decreasing the generation of intracellular reactive oxygen species (ROS). These two selenylated products were also more effective than LP in combating FB1-induced barrier disruption via increasing the transepithelial electric resistance (TEER), reducing the paracellular permeability, decreasing the mitochondrial membrane potential (MMP) loss, and maintaining cell barrier integrity by upregulating the tight-junction-related genes and proteins. FB1 caused cell oxidative stress and barrier dysfunction by activating the MAPK and mitochondrial apoptosis signaling pathways, while SeLP1 and SeLP2 could regulate the tMAPK- and apoptosis-related proteins to suppress the FB1-mediated activation of the two pathways. Overall, SeLP2 was observed to be more active than SeLP1 in the IEC-6 cells. In conclusion, the chemical selenylation of LP caused an activity enhancement to ameliorate the FB1-induced cell cytotoxicity and intestinal barrier disruption. Meanwhile, the increased selenylation of LP would endow the selenylated product SeLP2 with more activity.

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Section: Discussionmentioning

confidence: 99%

Longan Polysaccharides with Covalent Selenylation Combat the Fumonisin B1-Induced Cell Toxicity and Barrier Disruption in Intestinal Epithelial (IEC-6) Cells

Yu,

Zhao

2023

Nutrients

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“…For example, the Fusarium mycotoxins deoxynivalenol (DON) and fumonisin B1 (FB1) have been reported to directly affect the viability of phagocytic cells such as macrophages. Moreover, these mycotoxins can induce cellular apoptosis, inhibit proliferation, and impair the function of epithelial cells in vitro and in vivo [4,5], and can affect the expression of cytokines and chemokines, leading to immunosuppression and increased susceptibility to infections [6]. Several mycotoxins are also able to modulate the production of cytokines in different organs and/or cell types [7,8].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Immunomodulatory Effects of Fusarium Mycotoxins Using Bacterial Endotoxin-Stimulated Bovine Epithelial Cells and Macrophages in Co-Culture

Shandilya,

Sharma,

et al. 2023

Genes

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Mycotoxins are secondary metabolites produced by a variety of fungi that contaminate animal food and feeds and are capable of inducing a wide range of toxicities. Predictive in vitro models represent valuable substitutes for animal experiments to assess the toxicity of mycotoxins. The complexities of the interactions between epithelial and innate immune cells, vital for upholding barrier integrity and averting infections, remain inadequately understood. In the current study, a co-culture model of bovine epithelial cells (MAC-T) and macrophages (BoMac) was used to investigate the impact of exposure to Fusarium mycotoxins, namely deoxynivalenol (DON), zearalenone (ZEN), enniatin B (ENB), and beauvericin (BEA), on the inflammatory response elicited by the bacterial lipopolysaccharide (LPS) endotoxin. The MAC-T cells and BoMac were seeded on the apical side of a Transwell membrane and in the lower chamber, respectively, and mycotoxin exposure on the apical side of the membrane was carried out with the different mycotoxins (LC20; concentrations that elicited 20% cytotoxicity) for 48 h followed by an LPS immunity challenge for 24 h. The culture supernatants were collected from the basolateral compartment and these samples were submitted for cytokine/chemokine multiplex analysis. RNA-Seq analysis was performed using total RNA extracted from the MAC-T cells to acquire a more detailed insight into their cellular functions. The multiplex analysis indicated that IFN-γ, IL-1α, IL-8, and MCP-1 were significantly induced post-DON treatment when compared to control cells, and levels of IL-1α and IL-8 were enhanced significantly in all mycotoxin-treated groups post-LPS challenge. Analysis of the sequencing results showed that there were 341, 357, and 318 differentially expressed MAC-T cell genes that were up-regulated in the DON, ENB, and BEA groups, respectively. Gene ontology and pathway analysis revealed that these DEGs were significantly enriched in various biological processes and pathways related to inflammation, apoptosis signaling, and Wnt signaling. These results provide a comprehensive analysis of the co-culture cytokine/chemokine production and MAC-T cells’ gene expression profiles elicited by Fusarium mycotoxins, which further contributes to the understanding of early endotoxemia post-mycotoxin exposure.

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Integrating network pharmacology and experimental validation to explore the mechanisms of luteolin in alleviating fumonisin B1–induced intestinal inflammatory injury

Wen,

Han,

Chen

et al. 2024

Toxicon

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Effect of Fumonisin B1 on Proliferation and Apoptosis of Intestinal Porcine Epithelial Cells

Cited by 4 publications

References 33 publications

Longan Polysaccharides with Covalent Selenylation Combat the Fumonisin B1-Induced Cell Toxicity and Barrier Disruption in Intestinal Epithelial (IEC-6) Cells

Longan Polysaccharides with Covalent Selenylation Combat the Fumonisin B1-Induced Cell Toxicity and Barrier Disruption in Intestinal Epithelial (IEC-6) Cells

Evaluation of Immunomodulatory Effects of Fusarium Mycotoxins Using Bacterial Endotoxin-Stimulated Bovine Epithelial Cells and Macrophages in Co-Culture

Integrating network pharmacology and experimental validation to explore the mechanisms of luteolin in alleviating fumonisin B1–induced intestinal inflammatory injury

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