The G protein-coupled receptor FSHR-1 is required for the
            <i>Caenorhabditis elegans</i>
            innate immune response

Powell, Jennifer R.; Kim, Dennis H.; Ausubel, Frederick M.

doi:10.1073/pnas.0813048106

Cited by 116 publications

(146 citation statements)

References 36 publications

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“…Consistent with our results from the killing assays (Fig. 2C), six genes (T24B8.5, C32H11.1, C32H11.12, F35E12.5, C17H12.8, and K08D8.5) predicted to be strongly induced by P. aeruginosa (31,35,41) were either unchanged (C32H11.1) or repressed (T24B8.5, C32H11.12, F35E12.5, C17H12.8, and K08D8.5) by NCFM conditioning (Fig. 3A).…”

Section: Resultssupporting

confidence: 80%

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Caenorhabditis elegans Immune Conditioning with the Probiotic Bacterium Lactobacillus acidophilus Strain NCFM Enhances Gram-Positive Immune Responses

2012

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ABSTRACTAlthough the immune response ofCaenorhabditis elegansto microbial infections is well established, very little is known about the effects of health-promoting probiotic bacteria on evolutionarily conservedC. eleganshost responses. We found that the probiotic Gram-positive bacteriumLactobacillus acidophilusNCFM is not harmful toC. elegansand thatL. acidophilusNCFM is unable to colonize theC. elegansintestine. Conditioning withL. acidophilusNCFM significantly decreased the burden of a subsequentEnterococcus faecalisinfection in the nematode intestine and prolonged the survival of nematodes exposed to pathogenic strains ofE. faecalisandStaphylococcus aureus, including multidrug-resistant (MDR) isolates. Preexposure of nematodes toBacillus subtilisdid not provide any beneficial effects. Importantly,L. acidophilusNCFM activates key immune signaling pathways involved inC. elegansdefenses against Gram-positive bacteria, including the p38 mitogen-activated protein kinase pathway (via TIR-1 and PMK-1) and the β-catenin signaling pathway (via BAR-1). Interestingly, conditioning withL. acidophilusNCFM had a minimal effect on Gram-negative infection withPseudomonas aeruginosaorSalmonella entericaserovar Typhimurium and had no or a negative effect on defense genes associated with Gram-negative pathogens or general stress. In conclusion, we describe a new system for the study of probiotic immune agents and our findings demonstrate that probiotic conditioning withL. acidophilusNCFM modulates specificC. elegansimmunity traits.

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Section: Resultssupporting

confidence: 80%

“…Several immune response signaling pathways have been identified in C. elegans (12,15,28,31,32,48). Importantly, we found that C. elegans conditioning with the NCFM probiotic involves the p38 MAPK (via PMK-1) pathways, including the Toll/interleukin-1 receptor (TIR-1) pathway as well as the ␤-catenin (via BAR-1) signaling pathway (Fig.…”

Section: Discussionmentioning

confidence: 89%

Caenorhabditis elegans Immune Conditioning with the Probiotic Bacterium Lactobacillus acidophilus Strain NCFM Enhances Gram-Positive Immune Responses

2012

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“…3C). All three genes are known to be regulated by the p38 mitogen-activated protein kinase (MAPK) pathway (21,33). This suggested that exposure to PM may have provided protection from a subsequent PA14 infection by priming protective, p38-dependent immune responses.…”

Section: Resultsmentioning

confidence: 97%

Association with Soil Bacteria Enhances p38-Dependent Infection Resistance in Caenorhabditis elegans

et al. 2013

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The importance of our inner microbial communities for proper immune responses against invading pathogens is now well accepted, but the mechanisms underlying this protection are largely unknown. In this study, we used Caenorhabditis elegans to investigate such mechanisms. Since very little is known about the microbes interacting with C. elegans in its natural environment, we began by taking the first steps to characterize the C. elegans microbiota. We established a natural-like environment in which initially germfree, wild-type larvae were grown on enriched soil. Bacterial members of the adult C. elegans microbiota were isolated by culture and identified using 16S rRNA gene sequencing. Using pure cultures of bacterial isolates as food, we identified two, Bacillus megaterium and Pseudomonas mendocina, that enhanced resistance to a subsequent infection with the Gram-negative pathogen Pseudomonas aeruginosa. Whereas protection by B. megaterium was linked to impaired egg laying, corresponding to a known trade-off between fecundity and resistance, the mechanism underlying protection conferred by P. mendocina depended on weak induction of immune genes regulated by the p38 MAPK pathway. Disruption of the p38 ortholog, pmk-1, abolished protection. P. mendocina enhanced resistance to P. aeruginosa but not to the Gram-positive pathogen Enterococcus faecalis. Furthermore, protection from P. aeruginosa was similarly induced by a P. aeruginosa gacA mutant with attenuated virulence but not by a different C. elegans-associated Pseudomonas sp. isolate. Our results support a pivotal role for the conserved p38 pathway in microbiota-initiated immune protection and suggest that similarity between microbiota members and pathogens may play a role in such protection.

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“…The majority of this response appears to be a consequence of pathogenicity rather than direct recognition of PAMPs, because an attenuated P. aeruginosa gacA mutant failed to induce the majority of genes induced by the isogenic wild-type parent (14). Previously published work has shown that a portion of the C. elegans response to wild-type P. aeruginosa strain PA14 infection involves two parallel signaling pathways: the PMK-1 p38 MAPK pathway (14,16), a highly conserved immune pathway in metazoans, and a pathway containing the leucine-rich repeat G protein-coupled receptor FSHR-1 (17). However, the majority of genes transcriptionally activated by P. aeruginosa PA14 infection are induced independently of the PMK-1 p38 MAPK and FSHR-1 pathways, implicating additional pathways in the infection response.…”

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confidence: 99%

bZIP transcription factor zip-2 mediates an early response to Pseudomonas aeruginosa infection in Caenorhabditis elegans

Estes

Dunbar

Powell

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wildtype P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen.innate immunity | pathogenesis | intestine | host-pathogen interactions

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The G protein-coupled receptor FSHR-1 is required for the Caenorhabditis elegans innate immune response

Cited by 116 publications

References 36 publications

Caenorhabditis elegans Immune Conditioning with the Probiotic Bacterium Lactobacillus acidophilus Strain NCFM Enhances Gram-Positive Immune Responses

Caenorhabditis elegans Immune Conditioning with the Probiotic Bacterium Lactobacillus acidophilus Strain NCFM Enhances Gram-Positive Immune Responses

Association with Soil Bacteria Enhances p38-Dependent Infection Resistance in Caenorhabditis elegans

bZIP transcription factor zip-2 mediates an early response to Pseudomonas aeruginosa infection in Caenorhabditis elegans

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