scholarly journals Lifespan Extension in C. elegans Caused by Bacterial Colonization of the Intestine and Subsequent Activation of an Innate Immune Response

2019 ◽  
Vol 49 (1) ◽  
pp. 100-117.e6 ◽  
Author(s):  
Sandeep Kumar ◽  
Brian M. Egan ◽  
Zuzana Kocsisova ◽  
Daniel L. Schneider ◽  
John T. Murphy ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Bacterial Colonization ◽  
Innate Immune ◽  
Lifespan Extension ◽  
C Elegans ◽  
Subsequent Activation

scholarly journals Mitochondrial UPR negatively regulates wounding-induced innate immune response in C. elegans epidermis

2021 ◽  
Author(s):  
Jianzhi Zhao ◽  
Hongying Fu ◽  
Hengda Zhou ◽  
Xuecong Ren ◽  
Yuanyuan Wang ◽  
...  
Keyword(s):  
Immune Response ◽  
Signaling Pathways ◽  
Innate Immune Response ◽  
Tissue Damage ◽  
P38 Map Kinase ◽  
Innate Immune ◽  
Loss Of Function ◽  
C Elegans ◽  
Unfolded Protein ◽  
Protein Response

Tissue damage elicits a rapid innate immune response that is essential for efficient wound healing and survival of metazoans. It is well known that p38 MAPK kinase, TGF-β, and hemidesmosome signaling pathways have been involved in wounding-induced innate immunity in C. elegans. Here, we find that loss of function of ATFS-1 increased innate immune response while an elevated level of mitochondrial unfolded protein response (mitoUPR) inhibits the innate immune response upon epidermal wounding. Epidermal wounding triggers the nucleus export of ATFS-1 and inhibits themitoUPR in C. elegans epidermis. Moreover, genetic analysis suggests that ATFS-1 functions upstream of the p38 MAP kinase, TGF-β, and DAF-16 signaling pathways in regulating AMPs induction. Thus, our results suggest that the mitoUPR function as an intracellular signal required to fine-tune innate immune response after tissue damage.

scholarly journals Modulation of Host Innate Immune Response in the Bladder by Uropathogenic Escherichia coli

2007 ◽  
Vol 75 (11) ◽  
pp. 5353-5360 ◽  
Author(s):  
Benjamin K. Billips ◽  
Sarah G. Forrestal ◽  
Matthew T. Rycyk ◽  
James R. Johnson ◽  
David J. Klumpp ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Immune Response ◽  
Urinary Tract ◽  
Innate Immune Response ◽  
Bacterial Colonization ◽  
Innate Immune ◽  
Upec Strain ◽  
Chemokine Production ◽  
E Coli ◽  
K 12

ABSTRACT Uropathogenic Escherichia coli (UPEC), the most frequent cause of urinary tract infection (UTI), is associated with an inflammatory response which includes the induction of cytokine/chemokine secretion by urothelial cells and neutrophil recruitment to the bladder. Recent studies indicate, however, that UPEC can evade the early activation of urothelial innate immune response in vitro. In this study, we report that infection with the prototypic UPEC strain NU14 suppresses tumor necrosis factor alpha (TNF-α)-mediated interleukin-8 (CXCL-8) and interleukin-6 (CXCL-6) secretion from urothelial cell cultures compared to infection with a type 1 piliated E. coli K-12 strain. Furthermore, examination of a panel of clinical E. coli isolates revealed that 15 of 17 strains also possessed the ability to suppress cytokine secretion. In a murine model of UTI, NU14 infection resulted in diminished levels of mRNAs encoding keratinocyte-derived chemokine, macrophage inflammatory peptide 2, and CXCL-6 in the bladder relative to infection with an E. coli K-12 strain. Furthermore, reduced stimulation of inflammatory chemokine production during NU14 infection correlated with decreased levels of bladder and urine myeloperoxidase and increased bacterial colonization. These data indicate that a broad phylogenetic range of clinical E. coli isolates, including UPEC, may evade the activation of innate immune response in the urinary tract, thereby providing a pathogenic advantage.

Loss of DNase II function in the gonad is associated with a higher expression of antimicrobial genes in Caenorhabditis elegans

2015 ◽  
Vol 470 (1) ◽  
pp. 145-154 ◽  
Author(s):  
Hsiang Yu ◽  
Huey-Jen Lai ◽  
Tai-Wei Lin ◽  
Chang-Shi Chen ◽  
Szecheng J. Lo
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Caenorhabditis Elegans ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Dnase Ii ◽  
C Elegans ◽  
Elevated Expression

This study uncovered NUC-1 and CRN-7 function in germline apoptosis. Mutations of nuc-1 and crn-7 led to elevated expression of five innate-immunity-related genes and demonstrated that DNase II activity is associated with an innate immune response in C. elegans.

scholarly journals Analysis of the Caenorhabditis elegans innate immune response to Coxiella burnetii

2016 ◽  
Vol 23 (2) ◽  
pp. 111-127 ◽  
Author(s):  
James M Battisti ◽  
Lance A Watson ◽  
Myo T Naung ◽  
Adam M Drobish ◽  
Ekaterina Voronina ◽  
...  
Keyword(s):  
Immune Response ◽  
Caenorhabditis Elegans ◽  
Innate Immune Response ◽  
Coxiella Burnetii ◽  
Molecular Mechanisms ◽  
Q Fever ◽  
Innate Immune ◽  
Human Pathogens ◽  
C Elegans ◽  
Intestinal Distension

The nematode Caenorhabditis elegans is well established as a system for characterization and discovery of molecular mechanisms mediating microbe-specific inducible innate immune responses to human pathogens. Coxiella burnetii is an obligate intracellular bacterium that causes a flu-like syndrome in humans (Q fever), as well as abortions in domesticated livestock, worldwide. Initially, when wild type C. elegans (N2 strain) was exposed to mCherry-expressing C. burnetii (CCB) a number of overt pathological manifestations resulted, including intestinal distension, deformed anal region and a decreased lifespan. However, nematodes fed autoclave-killed CCB did not exhibit these symptoms. Although vertebrates detect C. burnetii via TLRs, pathologies in tol-1(–) mutant nematodes were indistinguishable from N2, and indicate nematodes do not employ this orthologue for detection of C. burnetii. sek-1(–) MAP kinase mutant nematodes succumbed to infection faster, suggesting that this signaling pathway plays a role in immune activation, as previously shown for orthologues in vertebrates during a C. burnetii infection. C. elegans daf-2(–) mutants are hyper-immune and exhibited significantly reduced pathological consequences during challenge. Collectively, these results demonstrate the utility of C. elegans for studying the innate immune response against C. burnetii and could lead to discovery of novel methods for prevention and treatment of disease in humans and livestock.

scholarly journals Heat shock enhances innate immune response to PG‐PS and M. tuberculosis in C. elegans

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Krishnaswamy Kannan ◽  
Xiaoxiao Wan ◽  
Aarthi Kannan ◽  
Deyu Fang ◽  
Robert Ortmann
Keyword(s):  
Immune Response ◽  
Heat Shock ◽  
Innate Immune Response ◽  
Innate Immune ◽  
C Elegans

scholarly journals Structural Damage in the C. elegans Epidermis Causes Release of STA-2 and Induction of an Innate Immune Response

Immunity ◽  
2015 ◽  
Vol 42 (2) ◽  
pp. 309-320 ◽  
Author(s):  
Yun Zhang ◽  
Wenna Li ◽  
Linfeng Li ◽  
Yuanbao Li ◽  
Rong Fu ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Structural Damage ◽  
Innate Immune ◽  
C Elegans

scholarly journals Caenorhabditis elegans microRNAs of the let-7 family act in innate immune response circuits and confer robust developmental timing against pathogen stress

2015 ◽  
Vol 112 (18) ◽  
pp. E2366-E2375 ◽  
Author(s):  
Zhiji Ren ◽  
Victor R. Ambros
Keyword(s):  
Immune Response ◽  
Caenorhabditis Elegans ◽  
P38 Mapk ◽  
Innate Immune Response ◽  
Regulatory Networks ◽  
Mapk Pathway ◽  
Regulation Of Gene Expression ◽  
Innate Immune ◽  
Developmental Timing ◽  
C Elegans

Animals maintain their developmental robustness against natural stresses through numerous regulatory mechanisms, including the posttranscriptional regulation of gene expression by microRNAs (miRNAs). Caenorhabditis elegans miRNAs of the let-7 family (let-7-Fam) function semiredundantly to confer robust stage specificity of cell fates in the hypodermal seam cell lineages. Here, we show reciprocal regulatory interactions between let-7-Fam miRNAs and the innate immune response pathway in C. elegans. Upon infection of C. elegans larvae with the opportunistic human pathogen Pseudomonas aeruginosa, the developmental timing defects of certain let-7-Fam miRNA mutants are enhanced. This enhancement is mediated by the p38 MAPK innate immune pathway acting in opposition to let-7-Fam miRNA activity, possibly via the downstream Activating Transcription Factor-7 (ATF-7). Furthermore, let-7-Fam miRNAs appear to exert negative regulation on the worm’s resistance to P. aeruginosa infection. Our results show that the inhibition of pathogen resistance by let-7 involves downstream heterochronic genes and the p38 MAPK pathway. These findings suggest that let-7-Fam miRNAs are integrated into innate immunity gene regulatory networks, such that this family of miRNAs modulates immune responses while also ensuring robust timing of developmental events under pathogen stress.

scholarly journals Identification of genes and molecular pathways involved in a C. elegans model of neuroborreliosis

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Ruben Prado ◽  
Gai-Linn Bessing ◽  
Nathaniel Snyder ◽  
Gurpalik Singh ◽  
Frank Yang ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Lyme Disease ◽  
Innate Immune Response ◽  
Genetic Model ◽  
Protein Aggregates ◽  
Neuronal Morphology ◽  
Innate Immune ◽  
Molecular Pathways ◽  
C Elegans

Background and Hypothesis: Lyme disease is caused by the spirochaete bacteria from the Borrelia species. Recent studies suggest that Lyme disease may be associated with dementia, brain atrophy, and protein aggregates that may be associated with the development of neurodegenerative diseases such as Parkinson’s disease (PD) and Alzheimers disease (AD). The molecular basis of the Borrelia-associated innate immune response and associated neuropathology is poorly defined.  A significant hindrance in dissecting these molecular components is the lack of facile in vivo genetic models to explore the mechanisms involved in the neuropathology. Here we hypothesize that the nematode C. elegans will be a useful model for Borrelia-associated innate immunity and neuropathology.  Project Methods: We utilized transcriptional reporters, transgenic animals, neuronal morphology analysis, RNAi, host defense pathways, AD- and PD-associated pathologies, and behavior assays to determine the effect that Borrelia has on C. elegans viability.  Results: C. elegans can be infected and survive using Borrelia as a food source, and the bacteria can induce highly conserved innate immune response pathways, and exacerbate PD-associated dopamine neuronal death in human A53T -synuclein-expressing animals. C. elegans models expressing AD-associated human A 1-42 also show significant movement defects and increased protein aggregates when exposed to Borrelia.  Conclusions and Potential Impact: This study further characterizes a novel genetic model for Borrelia-associated innate immunity and neuropathology. Incorporating C. elegans genetic screens, this model should allow us to identify mediators of the Borrelia-associated pathologies that should facilitate the identification of molecular pathways and potential therapeutic targets.

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