<i>Lactobacillus johnsonii</i>
            L531 ameliorates enteritis via elimination of damaged mitochondria and suppression of SQSTM1‐dependent mitophagy in a
            <i>Salmonella</i>
            infantis model of piglet diarrhea

Xia, Bing; Yu, Jiao; He, Ting; Liu, Xiao; Su, Jin-Hui; Wang, Qianqian; Wang, Jiufeng; Zhu, Yaohong

doi:10.1096/fj.201901445rrr

Cited by 32 publications

(40 citation statements)

References 49 publications

(110 reference statements)

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“…Furthermore, our previous study showed that Lactobacillus rhamnosus GG controlled S. Infantis infection by suppressing activation of intestinal epithelial cell autophagy in pigs [21]. More recently, we found that L. johnsonii prevented S. Infantis dissemination and ameliorated enteritis via suppression of autophagy in weaned pigs [22].…”

Section: Introductionmentioning

confidence: 80%

Butyrate-mediated autophagy inhibition limits cytosolic Salmonella Infantis replication in the colon of pigs treated with a mixture of Lactobacillus and Bacillus

Chu

Zhu

et al. 2020

Vet Res

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Probiotics as an effective and safe strategy for controlling Salmonella infection are much sought after, while autophagy is a central issue in eliminating intracellular pathogens of intestinal epithelial cells. In this study, an animal model of colitis has been developed by infecting weaned pigs orally with a strain of Salmonella Infantis in order to illuminate the potential efficacy of a mixture of Lactobacillus and Bacillus (CBB-MIX) in the resistance to Salmonella infection by regulating butyrate-mediated autophagy. We found that CBB-MIX alleviated S. Infantis-induced colitis and tissue damage. Autophagy markers ATG5, Beclin-1, and the LC3-II/I ratio were significantly enhanced by S. Infantis infection, while treatment with CBB-MIX suppressed S. Infantis-induced autophagy. Additionally, S. Infantis-induced colonic microbial dysbiosis was restored by this treatment, which also preserved the abundance of the butyrateproducing bacteria and the butyrate concentration in the colon. A Caco-2 cell model of S. Infantis infection showed that butyrate had the same effect as the CBB-MIX in restraining S. Infantis-induced autophagy activation. Further, the intracellular S. Infantis load assay indicated that butyrate restricted the replication of cytosolic S. Infantis rather than that in Salmonella-containing vacuoles. Suppression of autophagy by knockdown of ATG5 also attenuated S. Infantisinduced cell injury. Moreover, hyper-replication of cytosolic S. Infantis in Caco-2 cells was significantly decreased when autophagy was inhibited. Our data demonstrated that Salmonella may benefit from autophagy for cytosolic replication and butyrate-mediated autophagy inhibition reduced the intracellular Salmonella load in pigs treated with a probiotic mixture of Lactobacillus and Bacillus.

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Section: Introductionmentioning

confidence: 80%

Butyrate-mediated autophagy inhibition limits cytosolic Salmonella Infantis replication in the colon of pigs treated with a mixture of Lactobacillus and Bacillus

Chu

Zhu

et al. 2020

Vet Res

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“…Additionally, our recent study showed that administration of L. johnsonii L531 ameliorates enteritis of newly weaned piglets during S . infantis infection by promoting IgA secretion, reducing inflammation, and eliminating the damaged mitochondria [ 12 ]. In the present study, we found that pretreatment with L. johnsonii L531 restraints E. coli adhesion due to competitive exclusion and the production of inhibitory factors, thereby ameliorating E. coli –induced cell damages.…”

Section: Discussionmentioning

confidence: 99%

“…L. johnsonii L531 also ameliorates enteritis of newly weaned piglets during S . infantis infection [ 12 ]. However, whether L. johnsonii L531 could provide a new strategy for preventing and improving CM and the exact molecular mechanism underlying probiotic actions remains to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Lactobacillus johnsonii L531 Ameliorates Escherichia coli-Induced Cell Damage via Inhibiting NLRP3 Inflammasome Activity and Promoting ATG5/ATG16L1-Mediated Autophagy in Porcine Mammary Epithelial Cells

Zou

Wang

et al. 2020

Veterinary Sciences

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Escherichia coli (E. coli), a main mastitis-causing pathogen in sows, leads to mammary tissue damage. Here, we explored the effects of Lactobacillus johnsonii L531 on attenuating E. coli-induced inflammatory damage in porcine mammary epithelial cells (PMECs). L. johnsonii L531 pretreatment reduced E. coli adhesion to PMECs by competitive exclusion and the production of inhibitory factors and decreased E. coli-induced destruction of cellular morphology and ultrastructure. E. coli induced activation of NLRP3 inflammasome associated with increased expression of NLRP3, ASC, and cleaved caspase-1, however, L. johnsonii L531 inhibited E. coli-induced activation of NLRP3 inflammasome. Up-regulation of interleukin (Il)-1β, Il-6, Il-8, Il-18, tumor necrosis factor alpha, and chemokine Cxcl2 expression after E. coli infection was attenuated by L. johnsonii L531. E. coli infection inhibited autophagy, whereas L. johnsonii L531 reversed the inhibitory effect of E. coli on autophagy by decreasing the expression of autophagic receptor SQSTM1/p62 and increasing the expression of autophagy-related proteins ATG5, ATG16L1, and light chain 3 protein by Western blotting analysis. Our findings suggest that L. johnsonii L531 pretreatment restricts NLRP3 inflammasome activity and induces autophagy through promoting ATG5/ATG16L1-mediated autophagy, thereby protecting against E. coli-induced inflammation and cell damage in PMECs.

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“…The BeyoClick™ EdU Cell Proliferation Kit with Alexa Fluor 555 (EdU, Beyotime, Shanghai, China) was used to detect cell proliferation. After seeding in 24-well plates (5×10 3…”

Section: Edu Assaymentioning

confidence: 99%

“…Diarrhea is the main cause of death of newborn and suckling piglets, which brings enormous economic loss to the pig industry [1]. The occurrence of piglet diarrhea is related to genetic and improper management, especially the infection of pathogenic microorganisms, such as Escherichia coli [2], Salmonella [3], Clostridium perfringens [4][5][6], porcine epidemic diarrhea virus [7], etc. Therefore, it is necessary to search for molecular markers of diarrhea resistance and carry out porcine disease-resistant breeding.…”

Section: Introductionmentioning

confidence: 99%

ssc-miR-185 targets cell division cycle 42 and promotes the proliferation of intestinal porcine epithelial cell

Wang

Xie

et al. 2021

Anim Biosci

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Objective: microRNAs (miRNAs) can play a role in a variety of physiological and pathological regulation, and its role is achieved by regulating the expression of target genes. Our previous high-throughput sequencing found that ssc-miR-185 plays an important regulatory role in piglet diarrhea, but its specific target genes and functions in intestinal porcine epithelial cell (IPEC-J2) are still unclear. We intended to verify the target relationship between porcine miR-185 and cell division cycle 42 (CDC42) gene in IPEC-J2, and explored the effect of miR-185 on the proliferation of IPEC-J2 cells. Methods: The TargetScan, miRDB and miRanda softwares were used to predict the target genes of porcine miR-185, and CDC42 was selected as a candidate target gene. The CDC42-3'UTR-wild type (WT) and CDC42-3'UTR-mutant type (MUT) segments were successfully cloned into pmirGLO luciferase vector, and the luciferase activity was detected after co-transfection with miR-185 mimics and CDC42-3'UTR. The expression level of CDC42 was analyzed using qPCR and Western blot. The proliferation of IPEC-J2 was detected using CCK-8, MTT and EdU assays. Results: Double enzyme digestion and sequencing confirmed that CDC42-3'UTR-WT and CDC42-3'UTR-MUT were successfully cloned into pmirGLO luciferase reporter vector, and the luciferase activity was significantly reduced after co-transfection with miR-185 mimics and CDC42-3'UTR (WT). Further we found that the mRNA and protein expression level of CDC42 were down-regulated after transfection with miR-185 mimics, while the opposite trend was observed after transfection with miR-185 inhibitor (p < 0.01). In addition, the CCK-8, MTT and EdU results demonstrated that miR-185 promotes IPEC-J2 cells proliferation by targeting CDC42. Conclusion: These findings indicate that porcine miR-185 can directly target CDC42 and promote the proliferation of IPEC-J2 cells. However, the detailed regulatory mechanism of miR-185/CDC42 axis in piglets resistance to diarrhea is yet to be further investigation.

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Lactobacillus johnsonii L531 ameliorates enteritis via elimination of damaged mitochondria and suppression of SQSTM1‐dependent mitophagy in a Salmonella infantis model of piglet diarrhea

Cited by 32 publications

References 49 publications

Butyrate-mediated autophagy inhibition limits cytosolic Salmonella Infantis replication in the colon of pigs treated with a mixture of Lactobacillus and Bacillus

Butyrate-mediated autophagy inhibition limits cytosolic Salmonella Infantis replication in the colon of pigs treated with a mixture of Lactobacillus and Bacillus

Lactobacillus johnsonii L531 Ameliorates Escherichia coli-Induced Cell Damage via Inhibiting NLRP3 Inflammasome Activity and Promoting ATG5/ATG16L1-Mediated Autophagy in Porcine Mammary Epithelial Cells

ssc-miR-185 targets cell division cycle 42 and promotes the proliferation of intestinal porcine epithelial cell

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