Bacillus velezensis A2 Inhibited the Cecal Inflammation Induced by Zearalenone by Regulating Intestinal Flora and Short-Chain Fatty Acids

Cai, Jing; Wang, Nan; Chen, Jia; Wu, Aibo; Nepovimová, Eugenie; Vališ, Martin; Long, Miao; Wu, Weijie; Kuča, Kamil

doi:10.3389/fnut.2022.806115

Cited by 12 publications

(7 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The suppression of SCFA producing bacteria was confirmed with the decreased caecal SCFAs concentration in our study. Our finding is consistent with a previous study that revealed a significantly lower caecal SCFAs content in the ZEA-treated animal group [52]. Low abundance of SCFAs, major metabolites from gut microbiota, and SCFAs-producing bacteria are linked to colon cancer development [53].…”

Section: Discussionsupporting

confidence: 93%

“…Alteration in the microbial community are known to influence the development of diseases such as irritable bowel disease, obesity, liver disease and cancer [40][41][42]. Consistent with a previous study that revealed a significantly lower cecal SCFAs content in the ZEA-treated animal group [43], we observed reduced cecal SCFAs and SCFA-producing bacteria, Rikenella [44] and Rikenellaceae RC9 gut group, and the anti-inflammatory bacterium Candidatus Saccharimonas [35]. A low abundance of SCFAs, major metabolites from the gut microbiota, and SCFA-producing bacteria has been linked to colon cancer development [45].…”

Section: Discussionsupporting

confidence: 91%

See 1 more Smart Citation

Mechanistic insights into zearalenone-accelerated colorectal cancer in mice using integrative multi-omics approaches

Wang

Lee

et al. 2022

Preprint

View full text Add to dashboard Cite

Zearalenone (ZEA), a secondary metabolite from Fusarium fungi found in cereal-based foods, promotes the growth of colon, breast, and prostate cancers in vitro. However, the lack of animal studies hinders a deeper mechanistic understanding of the cancer promotive effect of ZEA. The aim of this study was to unveil the effect of ZEA on colon cancer progression and its underlying mechanism. Through integrative analyses of transcriptomics, metabolomics, metagenomics, and host phenotypes, we investigated the impact of a 4-week ZEA intervention on colorectal cancer in xenograft mice. Our results showed that a 4-week ZEA intervention increased the tumor weight twofold. ZEA exposure significantly increased the mRNA and protein levels of BEST4, DGKB and KI67, and the phosphorylation levels of ERK1/2 and AKT. Metabolomics analysis of the serum revealed the levels of amino acids, including histidine, arginine, citrulline and glycine decreased significantly in the ZEA group. Furthermore, ZEA lowered the alpha diversity of the gut microbiota and reduced the abundance of 9 genera, such as Tuzzerella and Rikenella, etc. Further association analysis indicated that Tuzzerella was negatively associated with the expression of BEST4 and DGKB genes, serum uric acid level and tumor weight. In addition, circulatory hippuric acid level was positively correlated with the tumor weight and the expression of oncogenic genes, including ROBO3, JAK3 and BEST4. Altogether, our results indicated that ZEA promoted colon cancer tumor progression through enhancing the BEST4/AKT/ERK1/2 pathway, lowering the circulatory amino acid concentration, alternating the gut microbiota composition, and suppressing the SCFA production.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 91%

Mechanistic insights into zearalenone-accelerated colorectal cancer in mice using integrative multi-omics approaches

Wang

Lee

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…The present results showed that the proportions of short-chain fatty acids-producers (SCFAs-producers), lactic acid bacteria (LAB), and digestive enzyme-producing bacteria were much higher in the LPC-supplemented groups. SCFAs-produces Faecalibacterium (especially F. prausnitzii ), an indicator of intestinal health, and Bacillus (especially B. velezensis ), which has been evidenced to be able to ameliorate intestinal inflammation [ 55 , 56 ], had comparatively higher proportion in turbot diets with LPC. Meanwhile, a recent study in turbot showed that the dietary Bacillus species enhanced the abundance of Ralstonia , which was also significantly positively correlated with immune parameters such as AKP and ACP [ 57 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of Lysophosphatidylcholine on Intestinal Health of Turbot Fed High-Lipid Diets

Luo

Liao

et al. 2022

Nutrients

View full text Add to dashboard Cite

An 8-week feeding trial was conducted, where turbot were fed four experimental diets, containing different LPC levels (0%, 0.1%, 0.25%, and 0.5%, named LPC0, LPC0.1, LPC0.25, and LPC0.5, respectively). The intestinal morphology results showed that there were no widened lamina propria and mixed inflammatory cells in the LPC-supplemented groups. Dietary LPC remarkably decreased the expression of TLRs (TLR3, TLR8, TLR9, and TLR22), MyD88, and signaling molecules (NF-κB, JNK, and AP-1). Similarly, diets with LPC supplementation markedly depressed the gene expression of NF-κB and JNK signaling pathway downstream genes (TNF-α, IL-1β, Bax, Caspase9, and Caspase-3). Furthermore, dietary LPC modified the intestinal microbial profiles, increasing the relative abundance of short-chain fatty acids-producers, lactic acid bacteria, and digestive enzyme-producing bacteria. Predictive functions of intestinal microbiota showed that turbot fed LPC diets had a relatively higher abundance of functions, such as lipid metabolism and immune system, but a lower abundance of functions, such as metabolic diseases and immune system diseases. The activities of intestinal acid phosphatase and alkaline phosphatase were also increased by dietary LPC. In conclusion, LPC supplementation could regulate the intestinal mucosal barrier via the TLR signaling pathway and alter the intestinal microbiota profile of turbot fed high-lipid diets.

show abstract

“…A2 inhibits the expression of inflammatory-related genes such as IL-6, TNF-α, and IL-1 β, alleviating the cellular inflammatory response induced by mycotoxins [ 40 ]. The excessive release of these inflammatory factors is associated with cell damage [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

Bacillus velezensis A2 Can Protect against Damage to IPEC-J2 Cells Induced by Zearalenone via the Wnt/FRZB/β-Catenin Signaling Pathway

Cai,

Yuan,

Sun

et al. 2024

Toxins

Self Cite

View full text Add to dashboard Cite

Zearalenone (ZEA) has adverse effects on human and animal health, and finding effective strategies to combat its toxicity is essential. The probiotic Bacillus velezensis A2 shows various beneficial physiological functions, including the potential to combat fungal toxins. However, the detailed mechanism by which the Bacillus velezensis A2 strain achieves this protective effect is not yet fully revealed. This experiment was based on transcriptome data to study the protective mechanism of Bacillus velezensis A2 against ZEA-induced damage to IPEC-J2 cells. The experiment was divided into CON, A2, ZEA, and A2+ZEA groups. This research used an oxidation kit to measure oxidative damage indicators, the terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) method to detect cell apoptosis, flow cytometry to determine the cell cycle, and transcriptome sequencing to screen and identify differentially expressed genes. In addition, gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were adopted to screen out relevant signaling pathways. Finally, to determine whether A2 can alleviate the damage caused by ZEA to cells, the genes and proteins involved in inflammation, cell apoptosis, cell cycles, and related pathways were validated using a quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot methods. Compared with the CON group, the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in the ZEA group increased significantly (p < 0.01), while the levels of antioxidant enzyme activity, total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-PX), total antioxidant capacity (T-AOC), and catalase (CAT) decreased significantly (p < 0.01). Compared with the ZEA group, the A2+ZEA group showed a significant decrease in ROS and MDA levels (p < 0.01), while the levels of T-SOD, GSH-PX, T-AOC, and CAT increased significantly (p < 0.01). TUNEL and cell cycle results indicated that compared with the ZEA group, the A2+ZEA group demonstrated a significant decrease in the cell apoptosis rate (p < 0.01), and the cell cycle was restored. Combining transcriptome data, qRT-PCR, and Western blot, the results showed that compared with the CON group, the mRNA and protein expression levels of Wnt10 and β-catenin increased significantly (p < 0.01), while the expression level of FRZB decreased significantly (p < 0.01); compared with the ZEA group, the expression levels of these mRNA and proteins were reversed. Bacillus velezensis A2 can increase the antioxidant level, reduce inflammatory damage, decrease cell apoptosis, and correct the cell cycle when that damage is being caused by ZEA. The protective mechanism may be related to the regulation of the Wnt/FRZB cell/β-catenin signaling pathway.

show abstract

Bacillus velezensis A2 Inhibited the Cecal Inflammation Induced by Zearalenone by Regulating Intestinal Flora and Short-Chain Fatty Acids

Cited by 12 publications

References 39 publications

Mechanistic insights into zearalenone-accelerated colorectal cancer in mice using integrative multi-omics approaches

Mechanistic insights into zearalenone-accelerated colorectal cancer in mice using integrative multi-omics approaches

Effects of Lysophosphatidylcholine on Intestinal Health of Turbot Fed High-Lipid Diets

Bacillus velezensis A2 Can Protect against Damage to IPEC-J2 Cells Induced by Zearalenone via the Wnt/FRZB/β-Catenin Signaling Pathway

Contact Info

Product

Resources

About