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Lanxin Yuan

Bio: Lanxin Yuan is an academic researcher from China Agricultural University. The author has contributed to research in topics: Phosphorylation & Autophagosome. The author has co-authored 3 publications.

Papers
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Journal ArticleDOI
17 Sep 2021
TL;DR: Wang et al. as mentioned in this paper established an IPEC-J2 cell model of S. Typhimurium infection, aiming to determine the protective effect of Lactobacillus johnsonii L531 pre-incubation, which inhibited the activation of the TLR4/NF-κB/NLRP3 signaling pathway and reduced the expression levels of pro-inflammatory cytokines.
Abstract: Salmonella Typhimurium (S. Typhimurium) is an aggressive zoonotic pathogen that causes enteritis and diarrhea. Antibiotic therapy is still the primary method at present. However, the increasing emergence of multi-drug resistant bacteria weakens the therapeutic efficacy of antibiotics. Probiotics have been widely studied as an alternative antibiotic therapy. In this study, we established an IPEC-J2 cell model of S. Typhimurium infection, aiming to determine the protective effect of Lactobacillus johnsonii L531 (L. johnsonii L531) on S. Typhimurium infection. As our data showed, S. Typhimurium infection resulted in a robust inflammatory response demonstrated by promoted protein levels of the inflammatory-related pathway (TLR4, MyD88, p-IκBα, and p-p65), increased cytokine levels of IL-6, IL-1β, IL-18, and TNF-α, and activated the NLRP3 inflammasome via promoting its assembly. However, L. johnsonii L531 pre-incubation inhibited the activation of the above inflammatory signaling pathways and reduced the expression levels of pro-inflammatory cytokines. In addition, L. johnsonii L531 alleviated the damage of S. Typhimurium to tight junctions ZO-1, Occludin, and Claudin-1. In summary, our findings suggested that L. johnsonii L531 alleviated S. Typhimurium-induced tight junction injury by inhibiting the TLR4/NF-κB/NLRP3 inflammasome signaling pathway.

9 citations

DOI
16 Nov 2021
TL;DR: In this paper, the effects of exopolysaccharides (EPS) from Bifidobacterium animalis subsp. lactis on ameliorating the damage of an intestinal porcine epithelial cell line (IPEC-J2) during EPEC infection were explored.
Abstract: Enteropathogenic Escherichia coli (EPEC) is a common zoonotic pathogen that causes acute infectious diarrhea. Probiotics like Bifidobacterium are known to help prevent pathogen infections. The protective effects of Bifidobacterium are closely associated with its secretory products exopolysaccharides (EPS). We explored the effects of the EPS from Bifidobacterium animalis subsp. lactis (B. lactis) on ameliorating the damage of an intestinal porcine epithelial cell line (IPEC-J2) during EPEC infection. Pretreatment with EPS alleviated EPEC-induced apoptosis through the restoration of cell morphology and the downregulation of protein expressions of cleaved-caspase 8, cleaved-caspase 3, and cleaved-PARP. EPS-mediated remission of apoptosis significantly improved cell viability during EPEC infection. EPEC infection also resulted in impaired autophagy, as demonstrated by decreased expressions of autophagy-related proteins Beclin 1, ATG5, and microtubule-binding protein light chain-3B (LC3B) and the increased expression of p62 through western blot analysis. However, EPS reversed these effects which indicated that EPS promoted autophagosome formation. Furthermore, EPS prevented the lysosome damage induced by EPEC as it enhanced lysosomal acidification and raised lysosome-associated protein levels, thus promoted autophagosome degradation. Our findings suggest that the amelioration of EPEC-induced cell damages by EPS is associated with the limitation of detrimental apoptosis and the promotion of autophagy flux.

6 citations

Journal ArticleDOI
TL;DR: In this article, Salmonella Infantis inhibited apoptosis of infected Caco-2 cells by phosphorylating Akt in a discontinuous manner: immediately 0.5 h after the invasion, then before peak cytosolic replication.
Abstract: Salmonella Infantis has emerged as a major clinical pathogen causing gastroenteritis worldwide in recent years. As an intracellular pathogen, Salmonella has evolved to manipulate and benefit from the cell death signaling pathway. In this study, we discovered that S. Infantis inhibited apoptosis of infected Caco-2 cells by phosphorylating Akt. Notably, Akt phosphorylation was observed in a discontinuous manner: immediately 0.5 h after the invasion, then before peak cytosolic replication. Single-cell analysis revealed that the second phase was only induced by cytosolic hyper-replicating bacteria at 3-4 hpi. Next, Akt-mediated apoptosis inhibition was found to be initiated by Salmonella SopB. Furthermore, Akt phosphorylation increased mitochondrial localization of Bcl-2 to prevent Bax oligomerization on the mitochondrial membrane, maintaining the mitochondrial network homeostasis to resist apoptosis. In addition, S. Infantis induced pyroptosis, as evidenced by increased caspase-1 (p10) and GSDMS-N levels. In contrast, cells infected with the ΔSopB strain displayed faster but less severe pyroptosis and had a less bacterial load. The results indicated that S. Infantis SopB mediated Akt phosphorylation delayed pyroptosis, but aggravated its severity. The wild-type strain also caused more severe diarrhea and intestinal inflammatory damage than the ΔSopB strain in mice. These findings revealed that S. Infantis delayed the cells death by intermittent activation of Akt, allowing sufficient time for replication, thereby causing more severe inflammation.

3 citations


Cited by
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Journal ArticleDOI
TL;DR: An updated status of knowledge regarding food bioactive compounds as NLRP3 inflammasome modulators is discussed, confirming the importance of the nutritional pattern (food model) as a whole rather than any single nutrient or functional compound.
Abstract: Inflammasomes are key intracellular multimeric proteins able to initiate the cellular inflammatory signaling pathway. NLRP3 inflammasome represents one of the main protein complexes involved in the development of inflammatory events, and its activity has been largely demonstrated to be connected with inflammatory or autoinflammatory disorders, including diabetes, gouty arthritis, liver fibrosis, Alzheimer’s disease, respiratory syndromes, atherosclerosis, and cancer initiation. In recent years, it has been demonstrated how dietary intake and nutritional status represent important environmental elements that can modulate metabolic inflammation, since food matrices are an important source of several bioactive compounds. In this review, an updated status of knowledge regarding food bioactive compounds as NLRP3 inflammasome modulators is discussed. Several chemical classes, namely polyphenols, organosulfurs, terpenes, fatty acids, proteins, amino acids, saponins, sterols, polysaccharides, carotenoids, vitamins, and probiotics, have been shown to possess NLRP3 inflammasome-modulating activity through in vitro and in vivo assays, mainly demonstrating an anti-NLRP3 inflammasome activity. Plant foods are particularly rich in important bioactive compounds, each of them can have different effects on the pathway of inflammatory response, confirming the importance of the nutritional pattern (food model) as a whole rather than any single nutrient or functional compound.

10 citations

Journal ArticleDOI
TL;DR:
Abstract: Enteric diseases caused by Salmonella are prevalent in poultry farming. With the forbiddance of antibiotics in feedstuff industry, Bacillus subtilis (B. subtilis) preparation as antibiotic alternatives against Salmonella infection has gained increasing attention recently. However, the protection modes of B. subtilis against Salmonella infection in broilers are strain-specific. In this study, probiotic B. subtilis LF11 significantly reduced diarrhea and mortality of broilers caused by Salmonella braenderup (S. braenderup) in spite of no inhibition effect on it in vitro. Here, the intestinal epithelial cells NCM460 were incubated to explore the protection of B. subtilis LF11 on intestinal epithelium against Salmonella. The results revealed that B. subtilis LF11 showed obvious exclusion activity with the decrease of adhesion and invasion of S. braenderup to NCM460 cells, accordingly with the increase of NCM460 cell survival compared with S. braenderup challenge alone. Meanwhile, RT-PCR and Western blot proved that the gene transcription and expression levels of four tight junction proteins in NCM 460 cells were upregulated, which was further confirmed by immunofluorescence observation. Besides, B. subtilis LF11 downregulated the gene transcription levels of the proinflammatory cytokines IL-6, IL-8, and TNF-α induced by S. braenderup H9812. ELISA analysis also verified that B. subtilis LF11 reduced the IL-8 production significantly. In general, B. subtilis LF11 has the ability to protect the intestinal epithelium against Salmonella infection by reducing the Salmonella adhesion and invasion, enhancing the intestinal barrier and attenuating the enterocyte inflammatory responses, and has the potential as probiotics to prevent enteric diseases in broilers.

9 citations

Journal ArticleDOI
TL;DR: JDYZF has a regulatory effect on the gut microbiota of AD rats, which may represent the basis for the anti-inflammatory effect of JDYZf.
Abstract: Background The Jiedu-Yizhi formula (JDYZF) is a Chinese herbal prescription used to treat Alzheimer's disease (AD). It was previously confirmed that JDYZF can inhibit the expression of pyroptosis-related proteins in the hippocampus of AD rats and inhibit gut inflammation in AD rats. Therefore, it is hypothesized that JDYZF has a regulatory effect on the gut microbiota. Methods In this study, an AD rat model was prepared by bilateral hippocampal injection of Aβ25-35 and AD rats received high, medium, and low doses of JDYZF orally for 8 weeks. The body weights of the AD rats were observed to assess the effect of JDYZF. The 16S rRNA sequencing technique was used to study the regulation of the gut microbiota by JDYZF in AD rats. Immunohistochemical staining was used to observe the expression levels of Caspase-1 and Caspase-11 in the hippocampus. Results JDYZF reduced body weight in AD rats, and this effect may be related to JDYZF regulating body-weight-related gut microbes. The 16S rRNA analysis showed that JDYZF increased the diversity of the gut microbiota in AD rats. At the phylum level, JDYZF increased the abundances of Bacteroidota and Actinobacteriota and decreased the abundances of Firmicutes, Campilobacterota, and Desulfobacterota. At the genus level, the abundances of Lactobacillus, Prevotella, Bacteroides, Christensenellaceae_R-7_group, Rikenellaceae_RC9_gut_group, and Blautia were increased and the abundances of Lachnospiraceae-NK4A136-group, Anaerobiospirillum, Turicibacter, Oscillibacter, Desulfovibrio, Helicobacter, and Intestinimonas were decreased. At the species level, the abundances of Lactobacillus johnsonii, Lactobacillus reuteri, and Lactobacillus faecis were increased and the abundances of Helicobacter rodentium and Ruminococcus_sp_N15.MGS-57 were decreased. Immunohistochemistry showed that JDYZF reduced the levels of Caspase-1- and Caspase-11-positive staining. Conclusion JDYZF has a regulatory effect on the gut microbiota of AD rats, which may represent the basis for the anti-inflammatory effect of JDYZF.

4 citations

Journal ArticleDOI
TL;DR: BaWeiBaiDuSan (BWBDS) was extracted from a formula of Panax ginseng C. A. Meyer, Lilium brownie F. E. Brown ex Miellez var. ex Redoute, Lonicera japonica Thunb, Hippophae rhamnoides Linn., Amygdalus Communis Vas, Platycodon grandiflorus (Jacq.) A. DC., and Cortex Phelloderdri as mentioned in this paper .

3 citations

Journal ArticleDOI
TL;DR: In this article , the authors used the piglet diarrhea model and the Caco2 cell model to explore the mechanism of probiotic Lactobacillus johnsonii L531 (L. Johnsonii) against S. Infantis infection.
Abstract: Salmonella enterica serovar Infantis (S. Infantis) is an intracellular bacterial pathogen. It is prevalent but resistant to antibiotics. Therefore, the therapeutic effect of antibiotics on Salmonella infection is limited. In this study, we used the piglet diarrhea model and the Caco2 cell model to explore the mechanism of probiotic Lactobacillus johnsonii L531 (L. johnsonii L531) against S. Infantis infection. L. johnsonii L531 attenuated S. Infantis-induced intestinal structural and cellular ultrastructural damage. The expression of NOD pathway-related proteins (NOD1/2, RIP2), autophagy-related key proteins (ATG16L1, IRGM), and endoplasmic reticulum (ER) stress markers (GRP78, IRE1) were increased after S. Infantis infection. Notably, L. johnsonii L531 pretreatment not only inhibited the activation of the above signaling pathways but also played an anti-S. Infantis infection role in accelerating autophagic degradation. However, RIP2 knockdown did not interfere with ER stress and the activation of autophagy induced by S. Infantis in Caco2 cells. Our data suggest that L. johnsonii L531 pretreatment alleviates the intestinal damage caused by S. Infantis by inhibiting NOD activation and regulating ER stress, as well as promoting autophagic degradation.

2 citations