Tiancheng Wang's research while affiliated with Shenyang Agricultural University and other places

Lactococcus garvieae (L. garvieae) is a pathogenic bacterium that is Gram-positive and catalase-negative (GPCN), and it is capable of growing in a wide range of environmental conditions. This bacterium is associated with significant mortality and losses in fisheries, and there are concerns regarding its potential as a zoonotic pathogen, given its presence in cattle and dairy products. While we have identified and characterized virulent strains of L. garvieae through phenotyping and molecular typing studies, their impact on mammary tissue remains unknown. This study aims to investigate the pathogenicity of strong and weak virulent strains of L. garvieae using in vivo mouse models. We aim to establish MAC-T cell model to examine potential injury caused by the strong virulent strain LG41 through the TLR2/NLRP3/NF-kB pathway. Furthermore, we assess the involvement of NLRP3 inflammasome-mediated pyroptosis in dairy mastitis by silencing NLRP3. The outcomes of this study will yield crucial theoretical insights into the potential mechanisms involved in mastitis in cows caused by the L. garvieae-induced inflammatory response in MAC-T cells.

Lactococcus lactis (L. lactis) is the primary organism for lactic acid bacteria (LAB) and is a globally recognized safe microorganism for the regulation of the intestinal micro-ecological balance of animals and improving the immune performance of the host. L. lactis is known to play a commercially important role in feed fortification, milk fermentation, and vaccine production, but pathogenic L. lactis has been isolated from many clinical cases in recent years, such as the brain of silver carp with Lactococcosis, the liver and spleen of diseased waterfowl, milk samples and padding materials with cow mastitis, and blood and urine from human patients with endocarditis. In dairy farming, where L. lactis has been used as a probiotic in the past, however, some studies have found that L. lactis can cause mastitis in cows, but the lack of understanding of the pathogenesis of mastitis in cows caused by L. lactis has become a new problem. The main objective of this review is to analyze the increasingly serious clinical mastitis caused by L. lactis and combined with the wide application of L. lactis as probiotics, to comprehensively discuss the characteristics and diversity of L. lactis.

Lactococcus garvieae ( L. garvieae ) is a pathogenic bacterium that is Gram-positive and catalase-negative (GPCN), and it is capable of growing in a wide range of environmental conditions. This bacterium is associated with significant mortality and losses in fisheries, and there are concerns regarding its potential as a zoonotic pathogen, given its presence in cattle and dairy products. While we have identified and characterized virulent strains of L. garvieae through phenotyping and molecular typing studies, their impact on mammary tissue remains unknown. This study aims to investigate the pathogenicity of strong and weak virulent strains of L. garvieae using in vivo mouse models. We aim to establish MAC-T cell model to examine potential injury caused by the strong virulent strain LG41 through the TLR2/NLRP3/NF-kB pathway. Furthermore, we assess the involvement of NLRP3 inflammasome-mediated pyroptosis in dairy mastitis by silencing NLRP3. The outcomes of this study will yield crucial theoretical insights into the potential mechanisms involved in mastitis in cows caused by the L. garvieae -induced inflammatory response in MAC-T cells.

Replacing antibiotics with probiotics has become an important way to safely and effectively prevent and treat some gastrointestinal diseases. This study was conducted to investigate whether Lactobacillus salivarius WZ1 (L.S) could reduce the inflammatory injury to the mouse jejunum induced by Escherichia coli (ETEC) K88. Forty Kunming mice were randomly divided into four groups with 10 mice in each group. From day 1 to day 14, the control group and the E. coli group were administered with normal saline each day, while the L.S group and the L.S + E. coli group were gavaged with Lactobacillus salivarius WZ1 1 × 108 CFU/mL each day. On the 15th day, the E. coli group and the L.S + E. coli group were intragastrically administered ETEC K88 1 × 109 CFU/mL and sacrificed 24 h later. Our results show that pretreatment with Lactobacillus salivarius WZ1 can dramatically protect the jejunum morphological structure from the changes caused by ETEC K88 and relieve the morphological lesions of the jejunum, inhibiting changes in the mRNA expressions of TNF-α, IL-1β and IL-6 and the protein expressions of TLR4, NF-κB and MyD88 in the intestinal tissue of mice caused by ETEC K88. Moreover, pretreatment with Lactobacillus salivarius WZ1 also increased the relative abundance of beneficial genera such as Lactobacillus and Bifidobacterium and decreased the abundance of harmful genera such as Ralstonia and Helicobacter in the gut. These results demonstrate that Lactobacillus salivarius WZ1 can inhibit the inflammatory damage caused by ETEC K88 in mouse jejunum by regulating the TLR4/NF-κB/MyD88 inflammatory pathway and gut microbiota.

Lactococcus garvieae (L. garvieae) is a pathogenic gram-positive, catalase-negative (GPCN) bacterium that causes bovine mastitis. A total of 49 L. garvieae isolates were identified from 1441 clinical mastitis (CM) samples. The pathogenic effects of L. garvieae were studied with two infection models: bovine mammary epithelial cells cultured in vitro and murine mammary infections in vivo. The overall farm prevalence was 15.5% (13/84 farms in 9/19 provinces) and sample prevalence was 3.40% (49/1441). Post-treatment somatic cell count (SCC) post L. garvieae infection was significantly higher than the other GPCN pathogens isolated, and the bacteriological cure fraction was 41.94% (13/31) after intramammary antibiotic treatment. All L. garvieae isolates were resistant to rifaximin, 12.24% of isolates were resistant to cephalexin, and 10.20% (5/49) were multidrug-resistant (MDR). The most prevalent virulence genes were Hemolysin 1 (hly1)(100%), Hemolysin 2 (hly2) (97.96%), NADH oxidase (NADHO) (100%), Superoxide dismutase (SOD) (100%), Adhesin Pav (Pav) (100%), Adhesin PsaA (PsaA) (100%), Enolase (eno) (100%), Adhesin cluster 1(AC1) (100%), Adhesin cluster 2 (AC2) (100%), and several exopolysaccharides. L. garvieae rapidly adhered to bovine mammary epithelial cells, resulting in an elevated lactate dehydrogenase release. Edema and congestion were observed in challenged murine mammary glands and bacteria were consistently isolated at 12, 24, 48, 72, and 120 h after infection. We concluded that L. garvieae had good adaptive ability in the bovine and murine mammary cells and tissue. Given the resistance profile, penicillin and ampicillin are potential treatments for CM cases caused by L. garvieae.

Aflatoxins are toxic secondary metabolites produced by Aspergillus fungi. The most toxic among them is Aflatoxin B1 (AFB1) which is known to have genotoxic, immunotoxic, teratogenic, carcinogenic, and mutagenic toxic effects (amongst others). The mechanisms responsible for its toxicity include the induction of oxidative stress, cytotoxicity, and DNAdamage. Studies have found that natural anti-oxidants can reduce the damage that AFB1 inflicts on the body by alleviating oxidative stress and inhibiting the biotransformation of AFB1. Therefore, this review outlines the latest progress in research on the use of natural anti-oxidants as antidotes to aflatoxin poisoning and their detoxification mechanisms. It also considers the problems that may possibly arise from their use and their application prospects. Our aim is to provide a useful reference for the prevention and treatment of AFB1 poisoning.

The mycotoxin zearalenone (ZEA) in food and feed seriously harms human and animal health. How to reduce its toxicity is an important direction of current research on food safety. This study aim to assess the effects of procyanidins (PC) on cell apoptosis caused by ZEA and to clarify the role of Nrf2 in the process. Swine testicle (ST) cells were treated with ZEA (57.5 μmol/L) and/or PC (10 mg/L) for 24 h. Cell viability was detected by CCK-8 assay. Cell apoptosis and the level of ROS were detected by flow cytometry. The expression levels of mRNA and protein was detected by qRT-PCR and western blotting. Our results showed that ZEA reduced the antioxidant capacity of the ST cells, induced the cell apoptosis and inhibited the gene and protein expression of Nrf2 and its downstream genes (ho-1,nqo1), while PC improved the cell antioxidant capacity, reduced the degree of ZEA-induced cell apoptosis and promoted the gene and protein expression of Nrf2 and its downstream genes. However, when the Nrf2 small molecule inhibitor ML385 was added, the ability of PC to inhibit ZEA-induced cell apoptosis and promote the expression of Nrf2 and its downstream genes were decreased. Our results demonstrated that ZEA induced oxidative stress and apoptosis of ST cells, which were alleviated by PC intervention via activating Nrf2 signaling pathway. This finding of this study provided a molecular basis for the clinical application of PC to prevent ZEN-caused reproductive toxicity.

Background: Bacillus coagulans has been widely used in food and feed additives, which can effectively inhibit the growth of harmful bacteria, improve intestinal microecological environment, promote intestinal development, and enhance intestinal function, but its probiotic mechanism is not completely clear. Aim: The aim of this study is to discuss the effect and mechanism of Bacillus coagulans TL3 on oxidative stress and inflammatory injury of cecum induced by LPS. Method: The Wistar rats were randomly divided into four groups, each containing 7 animals. Two groups were fed with basic diet (the LPS and control, or CON, groups). The remaining groups were fed with basic diet and either a intragastric administration high or low dose of B. coagulans, forming the HBC and LBC groups, respectively. The rats were fed normally for two weeks. On the 15th day, those in the LPS, HBC, and LBC groups were injected intraperitoneally with LPS-the rats in the CON group were injected intraperitoneally with physiological saline. After 4 hours, all the rats were anesthetized and sacrificed by cervical dislocation, allowing samples to be collected and labeled. The inflammatory and antioxidant cytokine changes of the cecum were measured, and the pathological changes of the cecum were observed, determining the cecal antioxidant, inflammation, and changes in tight junction proteins and analysis of intestinal flora. Result: The results show that LPS induces oxidative damage in the cecal tissues of rats and the occurrence of inflammation could also be detected in the serum. The Western blot results detected changes in the NF-κB- and Nrf2-related signaling pathways and TJ-related protein levels. Compared with the LPS group, the HBC group showed significantly downregulated levels of expression of Nrf2, NQO1, HO-1, GPX, and GCLC. The expression of TLR4, MYD88, NF-κB, IL-6, TNFα, and IL-1β was also significantly downregulated, while the expression of other proteins (ZO-1, occludin, and claudin-1) increased significantly. Bacillus coagulans TL3 was also found to increase the relative abundance of the beneficial bacterium Akkermansia muciniphila in the intestines. There is also a significant reduction in the number of harmful bacteria Escherichia coli and Shigella (Enterobacteriaceae). Conclusion: Bacillus coagulans TL3 regulates the TLR4/MyD88/NF-κB and Nrf2 signaling pathways in the cecal tissue of rats, protects the intestine from inflammation and oxidative damage caused by LPS, and inhibits the reproduction of harmful bacteria and promotes beneficial effects by regulating the intestinal flora bacteria grow, thereby enhancing intestinal immunity.

Aflatoxin B1(AFB1) widely exists in food and feed, which seriously endangers human and animal health. How to detoxify AFB1 is a research hotspot at present. This study attempts to use the Bacillus amyloliquefaciens B10, one of probiotics strain as the research object to ascertain whether it can alleviate the kidney injury induced by AFB1 in mice and its mechanism. Fifty-six mice were divided into four groups (control, AFB1, AFB1 + B10, and B10). The mice that received intragastric administration for 28 days were euthanised, and serum was collected for biochemical index detection with fresh kidney tissue taken for HE staining, TUNEL detection, and protein expression detection. Our results showed that the biochemical indices changed, significant pathological changes appeared, the number of apoptotic cells increased in the kidney tissue of the AFB1 group mice; the protein expressions of Nrf2, HO-1,AKT, P-AKT, and Bcl-2 in the AFB1 group were significantly decreased; the protein expressions of Keap-1, PTEN, Bax, Caspase-9, and Caspase-3 were significantly increased. After B. amyloliquefaciens B10 co-treatment, compared with the AFB1 group, the biochemical indices, pathological changes, and protein expressions were significantly reversed. The results indicated that B. amyloliquefaciens B10 can alleviate AFB1-induced kidney injury in mice.

Aflatoxin B1 is a mycotoxin that widely exists in feed and has a great impact on human and animal health. This study aimed to examine whether Bacillus amyloliquefaciens B10 protected against aflatoxin B1-induced cecal inflammation in mice. It was found that Bacillus amyloliquefaciens B10 could significantly improve the effects of AFB1 on body weight and intestinal inflammation of mice and enhance the expression of tight-junction protein. Compared with the CON group, the combination of AFB1 and B10 significantly increased the abundance of Actinobacteria and Bacilli in a collaborative manner, and significantly reduced the abundance of Ruminococcae, Lactobacillaceae and Clostridia. Meanwhile, the results showed that the abundance of Bacterides and Bacterdia in AFB1 + B10 group was significantly lower than that of AFB1 group, and the Firmicutes increased significantly. Bacillus amyloliquefaciens B10 can be used as a feed additive and alleviate cecal inflammation induced by AFB1 in mice by regulating intestinal flora.