Distinct Innate Immune Responses to Infection and Wounding in the C. elegans Epidermis

AbstractPathogen recognition and triggering pattern of host innate immune system is critical to understanding pathogen-host interaction. It is generally accepted that the microbial infection can be recognized by host via pattern-triggered immunity (PTI) or effector-triggered immunity (ETI) responses. Recently, non-PRR-mediated cellular surveillance systems have been reported as an important supplement strategy to PTI and ETI responses. However, the mechanism of how surveillance systems sense pathogens and trigger innate immune responses is largely unknown. In the present study, using Bacillus thuringiensis-Caenorhabditis elegans as a model, we found a new approach for surveillance systems to sense the pathogens through no-PPRs patterns. We reported C. elegans can monitor intracellular energy status through the mitochondrial surveillance system to triggered innate immune responses against pathogenic attack via AMP-activated protein kinase (AMPK). Consider that the mitochondria surveillance systems and AMPK are conserved components from worms to mammals, our study suggests that disrupting mitochondrial homeostasis to activate the immune system through AMPK-dependent pathways may widely existing in animals.

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The neuropeptide receptor NMUR-1 regulates the specificity of C. elegans innate immunity against pathogen infection

10.1101/2021.05.06.442992 ◽

2021 ◽

Author(s):

Phillip Wibisono ◽

Shawndra Wibisono ◽

Jan Watteyne ◽

Chia-Hui Chen ◽

Durai Sellegounder ◽

...

Keyword(s):

Innate Immunity ◽

Immune System ◽

Immune Responses ◽

Adaptive Immune System ◽

Innate Immune ◽

Innate Immune Responses ◽

Immune Genes ◽

C Elegans ◽

Adaptive Immune ◽

Functional Assays

A key question in current immunology is how the innate immune system generates high levels of specificity. Like most invertebrates, Caenorhabditis elegans does not have an adaptive immune system and relies solely on innate immunity to defend itself against pathogen attacks, yet it can still differentiate different pathogens and launch distinct innate immune responses. Here, we have found that functional loss of NMUR-1, a neuronal GPCR homologous to mammalian receptors for the neuropeptide neuromedin U, has diverse effects on C. elegans survival against various bacterial pathogens. Transcriptomic analyses and functional assays revealed that NMUR-1 modulates C. elegans transcription activity by regulating the expression of transcription factors, which, in turn, controls the expression of distinct immune genes in response to different pathogens. Our study has uncovered a molecular basis for the specificity of C. elegans innate immunity that could provide mechanistic insights into understanding the specificity of vertebrate innate immunity.

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Nuclear Hormone Receptor Regulation of MicroRNAs Controls Innate Immune Responses in C. elegans

PLoS Pathogens ◽

10.1371/journal.ppat.1003545 ◽

2013 ◽

Vol 9 (8) ◽

pp. e1003545 ◽

Cited By ~ 18

Author(s):

Feng Liu ◽

Chen-Xi He ◽

Li-Jun Luo ◽

Quan-Li Zou ◽

Yong-Xu Zhao ◽

...

Keyword(s):

Immune Responses ◽

Hormone Receptor ◽

Nuclear Hormone Receptor ◽

Innate Immune ◽

Receptor Regulation ◽

Innate Immune Responses ◽

C Elegans

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PKA/KIN-1 mediates innate immune responses to bacterial pathogens in Caenorhabditis elegans

Innate Immunity ◽

10.1177/1753425917732822 ◽

2017 ◽

Vol 23 (8) ◽

pp. 656-666 ◽

Cited By ~ 11

Author(s):

Yi Xiao ◽

Fang Liu ◽

Pei-ji Zhao ◽

Cheng-Gang Zou ◽

Ke-Qin Zhang

Keyword(s):

Innate Immunity ◽

Nervous System ◽

Caenorhabditis Elegans ◽

Immune Responses ◽

Innate Immune ◽

Autophagic Flux ◽

Innate Immune Responses ◽

C Elegans ◽

Downstream Effector ◽

Model Animal

The genetically tractable organism Caenorhabditis elegans is a powerful model animal for the study of host innate immunity. Although the intestine and the epidermis of C. elegans that is in contact with pathogens are likely to function as sites for the immune function, recent studies indicate that the nervous system could control innate immunity in C. elegans. In this report, we demonstrated that protein kinase A (PKA)/KIN-1 in the neurons contributes to resistance against Salmonella enterica infection in C. elegans. Microarray analysis revealed that PKA/KIN-1 regulates the expression of a set of antimicrobial effectors in the non-neuron tissues, which are required for innate immune responses to S. enterica. Furthermore, PKA/KIN-1 regulated the expression of lysosomal genes during S. enterica infection. Our results suggest that the lysosomal signaling molecules are involved in autophagy by controlling autophagic flux, rather than formation of autophagosomes. As autophagy is crucial for host defense against S. enterica infection in a metazoan, the lysosomal pathway also acts as a downstream effector of the PKA/KIN-1 signaling for innate immunity. Our data indicate that the PKA pathway contributes to innate immunity in C. elegans by signaling from the nervous system to periphery tissues to protect the host against pathogens.

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Faculty Opinions recommendation of Distinct innate immune responses to infection and wounding in the C. elegans epidermis.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1158667.618880 ◽

2009 ◽

Author(s):

Michel Labouesse

Keyword(s):

Immune Responses ◽

Innate Immune ◽

Innate Immune Responses ◽

C Elegans

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C. elegans monitor energy status to trigger innate immune responses via AMPK pathway against bacterial pathogens

10.21203/rs.3.rs-590514/v1 ◽

2021 ◽

Author(s):

Donghai Peng ◽

Shouyong Ju ◽

Hanqiao Chen ◽

Shaoying Wang ◽

Jian Lin ◽

...

Keyword(s):

Bacillus Thuringiensis ◽

Immune Responses ◽

Surveillance System ◽

Innate Immune ◽

Ion Leakage ◽

Surveillance Systems ◽

Innate Immune Responses ◽

Energy Status ◽

Microbial Infection ◽

C Elegans

Abstract Pathogen recognition and triggering pattern of host innate immune system is critical to understanding pathogen-host interaction. Cellular surveillance systems have been reported as an important strategy for the identification of microbial infection. In the present study, using Bacillus thuringiensis-Caenorhabditis elegans as a model, we found a new approach for surveillance systems to sense the pathogens. We report that Bacillus thuringiensis produced Cry5Ba, a classical PFTs, leading mitochondrial damage and energy imbalance by causing potassium ion leakage, instead of directly targeting mitochondria. Interestingly, C. elegans can monitor intracellular energy status through the mitochondrial surveillance system to triggered innate immune responses against pathogenic attack via AMP-activated protein kinase (AMPK). Obviously, it is common that pathogens produce toxins to cause potassium leakage. Our study indicate that the imbalance of energy status is a common result of pathogen infection.Besides. AMPK-dependent surveillance system can act as a new stratege for host to recognize and defense pathogens.

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Oral Immune Activation by Disgust and Disease-Related Pictures

Journal of Psychophysiology ◽

10.1027/0269-8803/a000143 ◽

2015 ◽

Vol 29 (3) ◽

pp. 119-129 ◽

Cited By ~ 4

Author(s):

Richard J. Stevenson ◽

Deborah Hodgson ◽

Megan J. Oaten ◽

Luba Sominsky ◽

Mehmet Mahmut ◽

...

Keyword(s):

Immune Response ◽

Immune Responses ◽

Innate Immune Response ◽

Negative Control ◽

Innate Immune ◽

Innate Immune Responses ◽

Immune Markers ◽

Before And After ◽

Secondary Analyses ◽

Image Set

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.

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