Cell Signaling of Caenorhabditis elegans in Response to Enterotoxigenic Escherichia coli Infection and Lactobacillus zeae Protection

Zhou, Mengzhou; Liu, Xiaozhen; Yu, Hai; X, Yin; Nie, Shaoping; Xie, Mingyong; Chen, W.; Gong, Joshua

doi:10.3389/fimmu.2018.01745

Cited by 30 publications

(48 citation statements)

References 46 publications

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“…To determine the cell signaling of mutant cat-2 in response to the supplementation of dopamine in the life-span assay, the gene expression of major components in the p38-MAPK ( tir-1, nsy-1, sek-1 , and pmk-1 ) and IGF-1/DAF-16 ( age-1 and daf-16 ) pathways, previously identified antimicrobial peptides ( lys-7, spp-1, abf-2, clec-85, clec-60 , and abf-3 ), and other reported defense molecules ( sod-3, dbl-1 , and skn-1 ) was examined with the method described previously (Zhou et al, 2014 , 2018 ). The experiment was carried out in three parallels.…”

Section: Resultsmentioning

confidence: 99%

“…The life-span assays of C. elegans were performed as described with slight modifications (Zhou et al, 2018 ). Synchronized C. elegans was transferred to NGM agar with E. coli OP50 at 25°C until it reached the L4 stage.…”

Section: Methodsmentioning

confidence: 99%

“…Lactobacillus zeae LB1 was one of the best potential probiotic bacteria. It provided the protection by inhibiting the gene expression of E. coli enterotoxins (Zhou et al, 2014 ) and also by regulating C. elegans cell signaling through the p38-MAPK and DAF/insulin/insulin-like growth factor (IGF) pathways to control the production of antimicrobial peptides and defensing molecules (Zhou et al, 2018 ). However, it is unknown if the olfactory preference and neurotransmitters such as serotonin and dopamine play a role in the protection offered by the Lactobacillus isolate.…”

Section: Introductionmentioning

confidence: 99%

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The Role of Neurotransmitters in the Protection of Caenorhabditis Elegans for Salmonella Infection by Lactobacillus

Liu

Jiang

et al. 2020

Front. Cell. Infect. Microbiol.

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Salmonellosis is a common foodborne disease. We previously reported the protection of Caenorhabditis elegans from Salmonella Typhimurium DT104 infection by Lactobacillus zeae LB1. However, the mechanism is not fully understood. C. elegans exhibits behavior plasticity when presented with diverse pathogenic or commensal bacteria. Whether it can exert approach avoidance to S . Typhimurium through altering its neurological activity remains to be determined. In the current study, both the wild type and mutants defective in serotonin or dopamine production of C. elegans were used to investigate olfactory preference of the nematode to L. zeae LB1, DT104, and Escherichia coli OP50 by choice assays, and its resistance to DT104 infection and the protection offered by L. zeae LB1 using a life-span assay. The expression of target genes in C. elegans was also examined by real-time quantitative PCR. Results showed that pre-exposure to L. zeae LB1 did not elicit aversive olfactory behavior of the nematode toward DT104. Both mutants tph-1 and cat-2 succumbed faster than the wild type when infected with DT104. While pre-exposure to L. zeae LB1 significantly increased the survival of both the wild type and mutant tph-1 , it provided no protection to mutant cat-2 . Supplementation of dopamine resulted in both the resistance of mutant cat-2 to S . Typhimurium infection and the protection from L. zeae LB1 to the same mutant. Gene expression data also supported the observations in the life-span assay. These results suggest that both serotonin and dopamine play a positive role in the host defense of C. elegans to S . Typhimurium infection and that the L. zeae LB1 protection is not dependent on modifying olfactory preference of the nematode but mediated by dopamine that may have involved the regulation of p38-mitogen-activated protein kinase and insulin/insulin-like growth factor signaling pathways.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The Role of Neurotransmitters in the Protection of Caenorhabditis Elegans for Salmonella Infection by Lactobacillus

Liu

Jiang

et al. 2020

Front. Cell. Infect. Microbiol.

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“…Still, other work in a nematode model of E . coli sepsis showed that only certain strains of Lactobacillus further increased MAPK activation during infection, resulting in better survival outcomes [ 43 ]. Further work is therefore needed to more fully understand the effect of Lactobacillus on this pathway as well as its downstream effect on pregnancy outcomes.…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus strains vary in their ability to interact with human endometrial stromal cells

Shiroda

Manning

2020

PLoS ONE

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The placental membranes that surround the fetus during pregnancy were suggested to contain a low abundance microbiota. Specifically, abundance of Lactobacillus , a probiotic and dominant member of the microbiome of the lower reproductive tract, has been shown to correlate with healthy, term pregnancies. We therefore sought to assess the interactions between four different Lactobacillus strains with immortalized decidualized endometrial cells (dT-HESCs), which were used as a model to represent the outermost layer of the placental membranes. Notably, we demonstrated that all four Lactobacillus strains could associate with dT-HESCs in vitro . L . crispatus was significantly more successful (p < 0.00005), with 10.6% of bacteria attaching to the host cells compared to an average of 0.8% for the remaining three strains. The four strains also varied in their ability to form biofilms. Dependent on media type, L . reuteri 6475 formed the strongest biofilms in vitro . To examine the impact on immune responses, levels of total and phosphorylated protein p38, a member of the Mitogen Activated Protein Kinase (MAPK) pathway, were examined following Lactobacillus association with dT-HESCs. Total levels of p38 were reduced to an average of 44% that of the cells without Lactobacillus (p < 0.05). While a trend towards a reduction in phosphorylated p38 was observed, this difference was not significant (p > 0.05). In addition, association with Lactobacillus did not result in increased host cell death. Collectively, these data suggest that varying types of Lactobacillus can attach to the outermost cells of the placental membranes and that these interactions do not contribute to inflammatory responses or host cell death. To our knowledge this is the first in vitro study to support the ability of Lactobacillus to interact with placental cells, which is important when considering its use as a potential probiotic within the reproductive tract.

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“…To elucidate the mechanisms involved in the action of Lcr35 ® against C. albicans, we studied the expression of seven C. elegans genes (Table 2) divided into three groups: daf-2 and daf-16 (insulin signaling pathway) involved in host longevity and antipathogenicity response, sek-1 and pmk-1 (p38 MAPK signaling pathway) which concern the immunity reaction as well as abf-2, cnc-4 and fipr-22/fipr-23 which encode antimicrobial proteins. The interest in targeting these genes has been demonstrated by various studies showing that the insulin and p38 MAPK pathways were involved in the pro-longevity properties of lactobacilli and bifidobacteria [12,[18][19][20], while the antimicrobial genes were involved in the anti-Candida effect [21]. In comparison with the E. coli OP50 control condition, we noted that Lcr35 ® induced an overexpression of daf-16 (p = 0.0004) and had no effect on daf-2 (p = 0.9459), while C. albicans tended to induce an up regulation of daf-2 (p = 0.0922) and a down-regulation of daf-16 (p = 0.4959).…”

Section: Modulation Of C Elegans Genes Expression Induced By Lcr35 ®mentioning

confidence: 99%

Curative Treatment of Candidiasis by the Live Biotherapeutic Microorganism Lactobacillus rhamnosus Lcr35® in the Invertebrate Model Caenorhabditis elegans: First Mechanistic Insights

et al. 2019

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The resistance of Candida albicans to conventional drug treatments, as well as the recurrence phenomena due to dysbiosis caused by antifungal treatments, have highlighted the need to implement new therapeutic methodologies. The antifungal potential of live biotherapeutic products (LBP) has already been demonstrated using preclinical models (cell cultures, laboratory animals). Understanding their mechanisms of action is strategic for the development of new therapeutics for humans. In this study, we investigated the curative anti-C. albicans properties of Lactobacillus rhamnosus Lcr35 ® using the in vitro Caco-2 cell and the in vivo Caenorhabditis elegans models. We showed that Lcr35 ® does inhibit neither the growth (p = 0.603) nor the biofilm formation (p = 0.869) of C. albicans in vitro. Lcr35 ® protects the animal from the fungal infection (+225% of survival, p < 2 × 10 -16 ) even if the yeast is detectable in its intestine. In contrast, the Lcr35 ® cell-free supernatant does not appear to have any antipathogenic effect. At the mechanistic level, the DAF-16/Forkhead Box O transcription factor is activated by Lcr35 ® and genes of the p38 MAP Kinase signaling pathway and genes involved in the antifungal response are upregulated in presence of Lcr35 ® after C. albicans infection. These results suggest that the LBM strain acts by stimulating its host via DAF-16 and the p38 MAPK pathway.

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Cell Signaling of Caenorhabditis elegans in Response to Enterotoxigenic Escherichia coli Infection and Lactobacillus zeae Protection

Cited by 30 publications

References 46 publications

The Role of Neurotransmitters in the Protection of Caenorhabditis Elegans for Salmonella Infection by Lactobacillus

The Role of Neurotransmitters in the Protection of Caenorhabditis Elegans for Salmonella Infection by Lactobacillus

Lactobacillus strains vary in their ability to interact with human endometrial stromal cells

Curative Treatment of Candidiasis by the Live Biotherapeutic Microorganism Lactobacillus rhamnosus Lcr35® in the Invertebrate Model Caenorhabditis elegans: First Mechanistic Insights

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