{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T13:03:30Z","timestamp":1787317410746,"version":"build-2736575974"},"reference-count":45,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2021,3,8]],"date-time":"2021-03-08T00:00:00Z","timestamp":1615161600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    <jats:italic>Salmonella typhimurium<\/jats:italic>\n                    DT104 infection causes the death of\n                    <jats:italic>Caenorhabditis elegans<\/jats:italic>\n                    , which can be prevented by certain\n                    <jats:italic>Lactobacillus<\/jats:italic>\n                    isolates. However, the molecular mechanisms of both the host response to the infection and the protection by\n                    <jats:italic>Lactobacillus<\/jats:italic>\n                    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\n                    <jats:italic>S. typhimurium<\/jats:italic>\n                    infection and protection from\n                    <jats:italic>Lactobacillus zeae<\/jats:italic>\n                    . The results indicated that the gene expression of\n                    <jats:italic>daf-16<\/jats:italic>\n                    in the DAF\/ insulin-like growth factor (DAF\/IGF) pathway,\n                    <jats:italic>ced-3<\/jats:italic>\n                    and\n                    <jats:italic>ced-9<\/jats:italic>\n                    in the programmed cell death (PCD) pathway,\n                    <jats:italic>lys-7, spp-1<\/jats:italic>\n                    , and\n                    <jats:italic>abf-3<\/jats:italic>\n                    for antimicrobial peptide production, and\n                    <jats:italic>bar-1<\/jats:italic>\n                    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\n                    <jats:italic>tir-1, sek-1<\/jats:italic>\n                    , and\n                    <jats:italic>pmk-1<\/jats:italic>\n                    in the p38 mitogen-activated protein kinase (MAPK) pathway and\n                    <jats:italic>clec-60, sod-3<\/jats:italic>\n                    , and\n                    <jats:italic>skn-1<\/jats:italic>\n                    for the production of other defense molecules was significantly suppressed by DT104. Pretreatment of the worms with\n                    <jats:italic>L. zeae<\/jats:italic>\n                    LB1 significantly upregulated the expression of almost all the tested genes except for\n                    <jats:italic>ced-3, ced-9, abf-2, age-1<\/jats:italic>\n                    , and\n                    <jats:italic>dbl-1<\/jats:italic>\n                    compared with the nematode infected with DT104 only. Mutants defective in the cell signaling or other defense molecules of\n                    <jats:italic>C. elegans<\/jats:italic>\n                    were either more susceptible (defective in\n                    <jats:italic>nsy-1, sek-1, pmk-1, ced-3, ced-9, skn-1<\/jats:italic>\n                    , or\n                    <jats:italic>daf-16<\/jats:italic>\n                    ) or more resistant (defective in\n                    <jats:italic>age-1<\/jats:italic>\n                    or\n                    <jats:italic>dbl-1<\/jats:italic>\n                    ) to DT104 infection than the WT except for the mutant defective in\n                    <jats:italic>sod-3<\/jats:italic>\n                    . Mutants defective in antimicrobial peptides (\n                    <jats:italic>lys-7<\/jats:italic>\n                    or\n                    <jats:italic>abf-3<\/jats:italic>\n                    ) were also more susceptible than the WT. In contrast, the mutant defective in\n                    <jats:italic>spp-1<\/jats:italic>\n                    became more resistant. When all the mutants were pretreated with\n                    <jats:italic>L. zeae<\/jats:italic>\n                    LB1, five mutants that are defective in\n                    <jats:italic>nsy-1, sek-1, pmk-1, abf-3<\/jats:italic>\n                    , or\n                    <jats:italic>lys-7<\/jats:italic>\n                    showed no response to the protection from LB1. These results suggest that\n                    <jats:italic>L. zeae<\/jats:italic>\n                    LB1 can regulate\n                    <jats:italic>C. elegans<\/jats:italic>\n                    cell signaling including the p38 MAPK pathway and downstream production of antimicrobial peptides and defense molecules to combat\n                    <jats:italic>Salmonella<\/jats:italic>\n                    infection.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2021.653205","type":"journal-article","created":{"date-parts":[[2021,3,7]],"date-time":"2021-03-07T23:19:43Z","timestamp":1615159183000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":15,"title":["Lactobacillus Regulates Caenorhabditis elegans Cell Signaling to Combat Salmonella 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