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The Microbial Zoo in the C. Elegans Intestine: Bacteria, Fungi and Viruses

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The Microbial Zoo in the C. Elegans Intestine: Bacteria, Fungi and Viruses viruses Review The Microbial Zoo in the C. elegans Intestine: Bacteria, Fungi and Viruses Hongbing Jiang and David Wang * Departments of Molecular Microbiology and Pathology & Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO 63110, USA; [email protected] * Correspondence: [email protected] Received: 7 January 2018; Accepted: 11 February 2018; Published: 14 February 2018 Abstract: C. elegans is an invaluable model organism that has been a driving force in many fundamental biological discoveries. However, it is only in the past two decades that it has been applied to host–pathogen interaction studies. These studies have been facilitated by the discoveries of natural microbes that infect C. elegans, including bacteria, fungi and viruses. Notably, many of these microbes share a common site of infection, the C. elegans intestine. Furthermore, the recent descriptions of a natural gut microbiota in C. elegans raise the possibility that this could be a novel model system for microbiome and trans-kingdom interaction studies. Here we review studies of C. elegans host–microbe interactions with a particular focus on the intestine. Keywords: host–pathogen interaction; C. elegans; intestine; bacteria; fungi; viruses; microbiome; trans-kingdom interactions 1. Preface Caenorhabidtitis elegans is a free living nematode found in soil, compost pits and rotting fruits. It was brought from the field to the lab by Sydney Brenner over 50 years ago [1] and has been used to address many fundamental biological questions. For example, the Caspase cell death pathway [2] and RNA interference [3] were first described in C. elegans and were later found to be conserved in many species including humans. There are many key features that have made C. elegans such a successful model including: A short lifecycle of approximately three days coupled to a hermaphroditic lifestyle that facilitates genetics; transparency of the body that enables live fluorescent imaging studies; a completely defined developmental cell lineage [4]; facile RNAi screening via readily available whole genome RNAi libraries; it was the first metazoan organism with a completely sequenced genome [5]; availability of many mutants and transgenic animals to the community via the C. elegans Genetics Center. As a differentiated multi-cellular organism, C. elegans mimics many aspects of mammalian physiology. Of particular relevance to many host–pathogen interactions is the C. elegans intestine, which as in higher eukaryotes, is the route of exposure and entry of many pathogens. The C. elegans intestine consists of 20 non-renewable epithelial cells, which make up the majority of its total body mass during development through the young adult stage. A key similarity between the C. elegans and human intestine is the presence of polarized epithelial cells with microvilli that are structurally attached to a terminal web composed of actin and intermediate filaments underneath the apical membrane [6,7]. The C. elegans intestine functions not only to assimilate nutrients, but also has the added function of detoxifying metabolites and toxins, like the liver in humans. It also consists of the first line of defense to invading pathogenic microbes. The intestinal lumen consists of the second-largest surface area in contact with the environment, besides the outer surface cuticle of the C. elegans body. Here, we review host–microbial interactions in C. elegans with a focus on those that occur in the intestine. Viruses 2018, 10, 85; doi:10.3390/v10020085 www.mdpi.com/journal/viruses Viruses 2018, 10, x FOR PEER REVIEW 2 of 11 Viruses 2018Here,, 10, we 85 review host–microbial interactions in C. elegans with a focus on those that occur in the2 of 12 intestine. 2. The2. TheC. C. elegans elegansMicrobiome Microbiome InIn nature natureC. elegansC. eleganslives lives in ain complex a complex environment, environment, feeding feeding on bacteria on bacteria and fungiand fungi that arethat present are inpresent soil, compost in soil, andcompost rotting and fruits.rotting Given fruits. thisGiven high this degree high degree of exposure of exposure to microbes, to microbes, it is it likelyis likely that inthat the wild,in the thewild,C. the elegans C. elegansintestine intestine may may be be populated populated by by many many differentdifferent micro-organisms. micro-organisms. In Inone one study,study, 18 18 species species of of bacteria bacteria were were identified identified inin thethe microbiota of of C.C. elegans elegans thatthat had had been been fed fed on on soil soil andand rotting rotting fruits fruits [8 [8].]. Furthermore, Furthermore,they they foundfound that the the natural natural microbiota microbiota conferred conferred protection protection from from pathogenicpathogenicP. P. aeruginosa aeruginosainfection. infection. In In 2016, 2016, threethree groupsgroups publ publishedished papers papers characterizing characterizing the the natural natural microbiomemicrobiome of ofC. elegansC. elegansand and found found very very similar similar habiting habiting bacteria bacteria species species in thein theC. elegansC. elegansintestine intestine from geographicallyfrom geographically different different samples samples over the over world the [ 9world–12]. The[9–12]. natural The natural microbiome microbiome studied studied was shown was to improveshownC. to elegansimprovegrowth, C. elegans resistance growth, toresistance stress and to stress relief and from relief pathogenic from pathogenic bacteria andbacteria fungi and infections. fungi Theseinfections. observations These parallelobservations recent parallel results inrecent the mouse, results demonstrating in the mouse, that demonstrating “wild” microbiota that “wild” provide microbiota provide a fitness advantage and increased resistance to environmental and infectious a fitness advantage and increased resistance to environmental and infectious insults [13]. insults [13]. 3. Bacteria–Host Interactions in the C. elegans Gut 3. Bacteria–Host Interactions in the C. elegans Gut Since most of the earliest studies of pathogen–host interactions in the C. elegans model focused Since most of the earliest studies of pathogen–host interactions in the C. elegans model focused on bacteria, it is natural that there are many reviews on this topic (Figure1)[ 7,14–18]. We will focus on bacteria, it is natural that there are many reviews on this topic (Figure 1) [7,14–18]. We will focus specifically on the intestinal response of C. elegans to pathogen infections (Table1). specifically on the intestinal response of C. elegans to pathogen infections (Table 1). Figure 1. Milestones relevant to host-pathogen interaction studies in C. elegans. Figure 1. Milestones relevant to host-pathogen interaction studies in C. elegans. Table 1. Pathogen–host interaction in the C. elegans intestine. Table 1. Pathogen–host interaction in the C. elegans intestine. Infection and Pathogenic Host Pathway and Kingdoms Pathogens Reference(s) InfectionMode and HostResponse Pathway andin the Response Intestine Kingdoms Pathogens Reference(s) Feeding;Pathogenic slow Mode killing by in the Intestine PMK-1, ZIP-2, FSHR-1 Feeding; slow killing by P. aeruginosa colonization and fast killing PMK-1, ZIP-2, FSHR-1 [19–22] P. aeruginosa colonization and fast killing dependent pathways [19–22] dependent pathways byby toxin toxin Feeding; killing by PMK-1-dependant Feeding; killing by PMK-1-dependant programmed S. entericaS. enterica colonization;colonization; LPS LPS as as programmed cell death [23[23]] cell death pathway virulence factor factor pathway Feeding;Feeding; colonizationcolonization causes causes S. marcescens distended intestine; LPS and DBL-1/TGF-β pathway [24] BacteriaBacteria distended intestine; LPS and S. marcescens hemolysin as virulence factors DBL-1/TGF-β pathway [24] hemolysin as virulence SEK-1 and NSY-1 dependent p38 Feeding; α-hemolysin as S. aureus factors MAP kinase pathway and TFEB [25,26] virulence factor mediated transcriptionalSEK-1 and NSY-1 response Feeding; colonization; dependent p38 MAP Feeding; α-hemolysin as S.S. aureus pyogenes hydrogen peroxide as kinaseNot pathway analyzed and TFEB [27[25,26]] virulence factor factor mediated transcriptional response Viruses 2018, 10, 85 3 of 12 Table 1. Cont. Infection and Host Pathway and Response Kingdoms Pathogens Reference(s) Pathogenic Mode in the Intestine CUL-6, SKR-3, 4, 5 ubiquitin N. parisii Feeding; intracellular infection [6,28–30] ligase pathways C. albicans Feeding; colonization; PMK-1/p-38 MAPK pathways [31] Fungi Feeding; colonization; laccase; polysaccharide capsule CED-1, C03F11.3 and ABL-1 C. neoformans [32,33] and/or melanization as dependent pathways virulence factors Infection of primary cell VSV RNA interference [34–36] culture or microinjection CED-3 and CED-4 Cell Vaccinia virus PEG permeabilization [37] death pathways Transgenic initiation of Viruses Flock house virus RNA interference [38–40] virus replication RNA interference CUL-6 ubiquitin-proteasome Orsay virus Feeding [41–52] degradation; STA-1 repression and CDE-1 PMK: P38 Map Kinase; ZIP: bZIP (basic Leucine Zipper) domain; FSHR: Follicle Stimulating Hormone Receptor; LPS: Lipopolysaccharide; DBL: Decapentaplegic/Bone morphogenic protein like; TGF: Transforming Growth Factor; SEK: SAPK/ERK Kinase; NSY: Neuronal Symmetry; MAP: Mitogen-Activated Protein; TFEB: Transcription factor EB; CUL: Cullin; SKR: Skp1 Related; CED: Cell death; ABL: Abelson Murine Leukemia; VSV: Vesicular Stomatitis Virus; PEG: Polyethylene Glycol;
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