Lactobacillus Regulates Caenorhabditis elegans Cell Signaling to Combat Salmonella Infection

Abstract

Salmonella typhimurium DT104 infection causes the death of Caenorhabditis elegans, which can be prevented by certain Lactobacillus isolates. However, the molecular mechanisms of both the host response to the infection and the protection by Lactobacillus are largely unclear. The present study has investigated the life-span and gene expression of both wild-type (WT) and mutants in some key components of cell signaling in response to S. typhimurium infection and protection from Lactobacillus zeae. The results indicated that the gene expression of daf-16 in the DAF/ insulin-like growth factor (DAF/IGF) pathway, ced-3 and ced-9 in the programmed cell death (PCD) pathway, lys-7, spp-1, and abf-3 for antimicrobial peptide production, and bar-1 involved in the production of other defense molecules was all significantly upregulated when the wild-type (WT) was subjected to DT104 infection. On the contrary, the gene expression of tir-1, sek-1, and pmk-1 in the p38 mitogen-activated protein kinase (MAPK) pathway and clec-60, sod-3, and skn-1 for the production of other defense molecules was significantly suppressed by DT104. Pretreatment of the worms with L. zeae LB1 significantly upregulated the expression of almost all the tested genes except for ced-3, ced-9, abf-2, age-1, and dbl-1 compared with the nematode infected with DT104 only. Mutants defective in the cell signaling or other defense molecules of C. elegans were either more susceptible (defective in nsy-1, sek-1, pmk-1, ced-3, ced-9, skn-1, or daf-16) or more resistant (defective in age-1 or dbl-1) to DT104 infection than the WT except for the mutant defective in sod-3. Mutants defective in antimicrobial peptides (lys-7 or abf-3) were also more susceptible than the WT. In contrast, the mutant defective in spp-1 became more resistant. When all the mutants were pretreated with L. zeae LB1, five mutants that are defective in nsy-1, sek-1, pmk-1, abf-3, or lys-7 showed no response to the protection from LB1. These results suggest that L. zeae LB1 can regulate C. elegans cell signaling including the p38 MAPK pathway and downstream production of antimicrobial peptides and defense molecules to combat Salmonella infection.

In Vitro Probiotic Evaluation of Saccharomyces boulardii with Antimicrobial Spectrum in a Caenorhabditis elegans Model

“…In this current study, the yeast KT000032 revealed substantial colonization efficiency at different feeding states with negligible differences. These results showed many similarities with the previous reports that showed that different lactic acid bacterial strains possess different attaching and colonization efficiency in C. elegans gut [ 30 ]. The correlation between colonization and hydrophobicity was reported by chelliah et al [ 31 ], but some studies showed no correlation between the two functional properties [ 32 ].…”

A Potential Probiotic Lactobacillus plantarum JBC5 Improves Longevity and Healthy Aging by Modulating Antioxidative, Innate Immunity and Serotonin-Signaling Pathways in Caenorhabditis elegans

“…Thus, we conclude that the feeding LPJBC5 activated skn-1 through the p38 MAPK signaling pathway to extend longevity in worms. This result is in accordance to the recent study by Zhou et al [ 60 ].…”

In vivo investigation of Lcr35® anti-candidiasis properties in Caenorhabditis elegans reveals the involvement of highly conserved immune pathways

“…Furthermore, loss-of-function mutants for the nsy-1, sek-1, pmk-1, abf-3 and lys-7 genes are insensitive to the antipathogenic effect of L. zeae. According to the authors, these results suggest the bacterium can regulate the host cell signaling via p38 MAPK pathway (Zhou et al, 2021). A similar conclusion was also advanced by the work of Dinić et al (2021) which showed that administration of the heat-inactivated probiotic strain Lactobacillus curvatus BGMK2-41 induced a PMK-1/p38 MAPK-dependent transcription of C-type lectins (clec-85, clec-172), lysozymes (lys-1, lys-3, lys-5, lys-8) and tight junction protein CLC-1.…”

“…Current work has enabled us to demonstrate that daf-16 and sek-1 functionalities are required for L. rhamnosus Lcr35 ® to exert its anti-C. albicans activity, in knockout mutants for these genes, the protective effect being abolished. Recently, Zhou et al (2021) investigated the anti-Salmonella Typhimurium DT104 capacities of Lactobacillus zeae LB1 using a preventive approach. They thus highlighted the overexpression of genes such as daf-16 (insulin pathway), tir-1, sek-1 and pmk-1 (p38 MAPK pathway) and clec-60, sod-3 and skn-1 (other defense molecules) in the presence of the lactobacillus.…”