scholarly journals Parasitoid wasp venom targets host immune cell production in a Drosophila-parasitoid interaction

2020 ◽  
Author(s):  
Jordann E. Trainor ◽  
KR Pooja ◽  
Nathan T. Mortimer
Keyword(s):  
Immune Cell ◽  
Sequence Data ◽  
Parasitoid Wasp ◽  
National Institutes Of Health ◽  
Medical Sciences ◽  
Host Signaling ◽  
Jnk Signaling Pathway ◽  
Host Parasite ◽  
Host Immune Cell ◽  
Venom Proteins

AbstractThe interactions between Drosophila melanogaster and the parasitoid wasps that infect Drosophila species provide an important model for understanding host-parasite relationships. Following parasitoid infection, D. melanogaster larvae mount a response in which immune cells (hemocytes) form a capsule around the wasp egg, which then melanizes leading to death of the parasitoid. Previous studies have found that host hemocyte load, the number of hemocytes available for the encapsulation response, and the production of lamellocytes, an infection induced hemocyte type, are major determinants of host resistance. Parasitoids have evolved various virulence mechanisms to overcome the immune response of the D. melanogaster host, including both active immune suppression by venom proteins and passive immune evasive mechanisms. We find that a previously undescribed parasitoid species, Asobara sp. AsDen, utilizes an active virulence mechanism to infect D. melanogaster hosts. Asobara sp. AsDen infection inhibits host hemocyte expression of msn, a member of the JNK signaling pathway, which plays a role in lamellocyte production. Asobara sp. AsDen infection restricts the production of lamellocytes as assayed by hemocyte cell morphology and altered msn expression. Our findings suggest that Asobara sp. AsDen venom targets host signaling to suppress immunity.DeclarationsFundingThis work was supported by the National Institute of General Medical Sciences of the National Institutes of Health under Award Number R35GM133760.Availability of data and materialSequence data has been deposited in GenBank under accession # MT498809. Custom BLAST databases are available on request to corresponding author.Authors’ contributionsConceived of or designed study: J.E.T., N.T.M.; Performed research: J.E.T., P.K.; Analyzed data: J.E.T., P.K., N.T.M.; Wrote the paper: J.E.T., P.K., N.T.M.

scholarly journals Immune Cell Production Is Targeted by Parasitoid Wasp Virulence in a Drosophila–Parasitoid Wasp Interaction

Pathogens ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 49
Author(s):  
Jordann E. Trainor ◽  
Pooja KR ◽  
Nathan T. Mortimer
Keyword(s):  
Immune Cells ◽  
Immune Cell ◽  
Parasitoid Wasp ◽  
Parasitoid Wasps ◽  
Parasitoid Species ◽  
Jnk Signaling ◽  
Host Signaling ◽  
Jnk Signaling Pathway ◽  
Host Parasite ◽  
Venom Proteins

The interactions between Drosophila melanogaster and the parasitoid wasps that infect Drosophila species provide an important model for understanding host–parasite relationships. Following parasitoid infection, D. melanogaster larvae mount a response in which immune cells (hemocytes) form a capsule around the wasp egg, which then melanizes, leading to death of the parasitoid. Previous studies have found that host hemocyte load; the number of hemocytes available for the encapsulation response; and the production of lamellocytes, an infection induced hemocyte type, are major determinants of host resistance. Parasitoids have evolved various virulence mechanisms to overcome the immune response of the D. melanogaster host, including both active immune suppression by venom proteins and passive immune evasive mechanisms. We identified a previously undescribed parasitoid species, Asobara sp. AsDen, which utilizes an active virulence mechanism to infect D. melanogaster hosts. Asobara sp. AsDen infection inhibits host hemocyte expression of msn, a member of the JNK signaling pathway, which plays a role in lamellocyte production. Asobara sp. AsDen infection restricts the production of lamellocytes as assayed by hemocyte cell morphology and altered msn expression. Our findings suggest that Asobara sp. AsDen infection alters host signaling to suppress immunity.

scholarly journals Improved Genome Assembly and Annotation of the Soybean Aphid (Aphis glycines Matsumura)

2020 ◽  
Vol 10 (3) ◽  
pp. 899-906 ◽  
Author(s):  
Thomas C. Mathers
Keyword(s):  
Genome Assembly ◽  
Sequence Data ◽  
Parasitoid Wasp ◽  
Single Copy ◽  
Aphid Species ◽  
Soybean Aphid ◽  
Aphis Glycines ◽  
Data Sets ◽  
Conserved Genes ◽  
Long Read

Aphids are an economically important insect group due to their role as plant disease vectors. Despite this economic impact, genomic resources have only been generated for a small number of aphid species. The soybean aphid (Aphis glycines Matsumura) was the third aphid species to have its genome sequenced and the first to use long-read sequence data. However, version 1 of the soybean aphid genome assembly has low contiguity (contig N50 = 57 Kb, scaffold N50 = 174 Kb), poor representation of conserved genes and the presence of genomic scaffolds likely derived from parasitoid wasp contamination. Here, I use recently developed methods to reassemble the soybean aphid genome. The version 2 genome assembly is highly contiguous, containing half of the genome in only 40 scaffolds (contig N50 = 2.00 Mb, scaffold N50 = 2.51 Mb) and contains 11% more conserved single-copy arthropod genes than version 1. To demonstrate the utility of this improved assembly, I identify a region of conserved synteny between aphids and Drosophila containing members of the Osiris gene family that was split over multiple scaffolds in the original assembly. The improved genome assembly and annotation of A. glycines demonstrates the benefit of applying new methods to old data sets and will provide a useful resource for future comparative genome analysis of aphids.

Description of the immature stages of the Neotropical whirligig beetle Gyrinus (Neogyrinus) rozei Ochs, 1953 (Coleoptera: Gyrinidae) and first report of the parasitoid wasp Melanosmicra sp. (Hymenoptera: Chalcididae) on a Gyrinus species

Zootaxa ◽  
2020 ◽  
Vol 4732 (1) ◽  
pp. 99-116
Author(s):  
DANIARA COLPANI ◽  
CÉSAR JOÃO BENETTI ◽  
NEUSA HAMADA ◽  
VANDERLY ANDRADE-SOUZA ◽  
KARINE SCHOENINGER ◽  
...  
Keyword(s):  
Dna Sequence ◽  
Sequence Data ◽  
Parasitoid Wasp ◽  
First Record ◽  
The Body ◽  
Immature Stages ◽  
Cytochrome Oxidase Subunit ◽  
Dna Sequence Data ◽  
Gene Coi ◽  
Northern Brazil

In most species of Gyrinidae, the immature stages are unknown, especially due to the difficulty in collecting the juveniles and assigning them to a particular species. Molecular association is a feasible technique that may solve this problem. Recent studies have used DNA sequence data, specifically the gene cytochrome oxidase subunit I (COI), to associate immature and adult stages, thus enabling the description of the former. The objectives of this study were (1) to describe and illustrate the immature stages of Gyrinus (Neogyrinus) rozei Ochs, 1953 including morphometric, chaetotaxic and bionomic information, and (2) to assess the usefulness of the gene COI to associate immatures and adults of Gyrinus. The studied specimens were collected in Roraima state, northern Brazil. The association of immature and adult stages was done either by rearing adults under laboratory conditions or by using DNA sequence data (COI). Eggs were described based on scanning electron microscopy; they are distinguished mainly by several features of chorion, micropyle and reticulation. Larvae of G. (N.) rozei can be distinguished from those of other Neotropical Gyrinidae by a combination of several characters, including the stipes with five robust hook-like additional setae on the dorsointernal margin, and the lacinia roughly hook-shaped. The pupa is similar to that of G. argentinus Steinhel, 1869, except for the number of setae on the body. The first record of the parasitoid wasp Melanosmicra sp. (Hymenoptera: Chalcididae) on a Gyrinus species is also provided. 

scholarly journals Translational impact of NIH-funded nonhuman primate research in transplantation

2019 ◽  
Vol 11 (500) ◽  
pp. eaau0143 ◽  
Author(s):  
Stuart J. Knechtle ◽  
Julia M. Shaw ◽  
Bernhard J. Hering ◽  
Kristy Kraemer ◽  
Joren C. Madsen
Keyword(s):  
Clinical Trials ◽  
Cell Therapy ◽  
Immune Responses ◽  
Nonhuman Primate ◽  
Immune Cell ◽  
National Institutes Of Health ◽  
Primate Research ◽  
Costimulation Blockade ◽  
Hematopoietic Chimerism ◽  
New Treatments

The National Institutes of Health (NIH) has long supported using nonhuman primate (NHP) models for research on kidney, pancreatic islet, heart, and lung transplantation. The primary purpose of this research has been to develop new treatments for down-modulating or preventing deleterious immune responses after transplantation in human patients. Here, we discuss NIH-funded NHP studies of immune cell depletion, costimulation blockade, regulatory cell therapy, desensitization, and mixed hematopoietic chimerism that either preceded clinical trials or prevented the human application of therapies that were toxic or ineffective.

Towards a comprehensive view of the primary structure of venom proteins from the parasitoid wasp Pimpla hypochondriaca

2004 ◽  
Vol 34 (6) ◽  
pp. 565-571 ◽  
Author(s):  
Neil M Parkinson ◽  
Christine Conyers ◽  
Jeff Keen ◽  
Alan MacNicoll ◽  
Ian Smith ◽  
...  
Keyword(s):  
Primary Structure ◽  
Parasitoid Wasp ◽  
Comprehensive View ◽  
Venom Proteins

scholarly journals Immune Evasion Strategies of Schistosomes

2021 ◽  
Vol 11 ◽  
Author(s):  
Jacob R. Hambrook ◽  
Patrick C. Hanington
Keyword(s):  
Immune Evasion ◽  
Immune Cell ◽  
Molecular Mimicry ◽  
Life Cycles ◽  
Host Responses ◽  
Immune Recognition ◽  
Factors Affecting ◽  
Cell Functions ◽  
Treatment Plans ◽  
Host Parasite

Human schistosomes combat the unique immune systems of two vastly different hosts during their indirect life cycles. In gastropod molluscs, they face a potent innate immune response composed of variable immune recognition molecules and highly phagocytic hemocytes. In humans, a wide variety of innate and adaptive immune processes exist in proximity to these parasites throughout their lifespan. To survive and thrive as the second most common parasitic disease in humans, schistosomes have evolved many techniques to avoid and combat these targeted host responses. Among these techniques are molecular mimicry of host antigens, the utilization of an immune resistant outer tegument, the secretion of several potent proteases, and targeted release of specific immunomodulatory factors affecting immune cell functions. This review seeks to describe these key immune evasion mechanisms, among others, which schistosomes use to survive in both of their hosts. After diving into foundational observational studies of the processes mediating the establishment of schistosome infections, more recent transcriptomic and proteomic studies revealing crucial components of the host/parasite molecular interface are discussed. In order to combat this debilitating and lethal disease, a comprehensive understanding of schistosome immune evasion strategies is necessary for the development of novel therapeutics and treatment plans, necessitating the discussion of the numerous ways in which these parasitic flatworms overcome the immune responses of both hosts.

scholarly journals Sympatric versus allopatric evolutionary contexts shape differential immune response in Biomphalaria / Schistosoma interaction

2018 ◽  
Author(s):  
Anaïs Portet ◽  
Silvain Pinaud ◽  
Cristian Chaparro ◽  
Richard Galinier ◽  
Nolwenn M. Dheilly ◽  
...  
Keyword(s):  
Immune Response ◽  
Life History ◽  
Schistosoma Mansoni ◽  
Local Adaptation ◽  
Cellular Response ◽  
Life History Traits ◽  
Immune Cell ◽  
Helminth Parasites ◽  
Geographic Variations ◽  
Host Parasite

AbstractSelective pressures between hosts and their parasites can result in reciprocal evolution or adaptation of specific life history traits. Local adaptation of resident hosts and parasites should lead to increase parasite infectivity/virulence (higher compatibility) when infecting hosts from the same location (in sympatry) than from a foreign location (in allopatry). Analysis of geographic variations in compatibility phenotypes is the most common proxy used to infer local adaptation. However, in some cases, allopatric host-parasite systems demonstrate similar or greater compatibility than in sympatry. In such cases, the potential for local adaptation remains unclear. Here, we study the interaction between Schistosoma and its vector snail Biomphalaria in which such discrepancy in local versus foreign compatibility phenotype has been reported. Herein, we aim at bridging this gap of knowledge by comparing life history traits (immune cellular response, host mortality, and parasite growth) and molecular responses in highly compatible sympatric and allopatric Schistosoma/Biomphalaria interactions originating from different geographic localities (Brazil, Venezuela and Burundi). We found that despite displaying similar prevalence phenotypes, sympatric schistosomes triggered a rapid immune suppression (dual-RNAseq analyses) in the snails within 24h post infection, whereas infection by allopatric schistosomes (regardless of the species) was associated with immune cell proliferation and triggered a non-specific generalized immune response after 96h. We observed that, sympatric schistosomes grow more rapidly. Finally, we identify miRNAs differentially expressed by Schistosoma mansoni that target host immune genes and could be responsible for hijacking the host immune response during the sympatric interaction. We show that despite having similar prevalence phenotypes, sympatric and allopatric snail-Schistosoma interactions displayed strong differences in their immunobiological molecular dialogue. Understanding the mechanisms allowing parasites to adapt rapidly and efficiently to new hosts is critical to control disease emergence and risks of Schistosomiasis outbreaks.Author summarySchistosomiasis, the second most widespread human parasitic disease after malaria, is caused by helminth parasites of the genus Schistosoma. More than 200 million people in 74 countries suffer from the pathological, and societal consequences of this disease. To complete its life cycle, the parasite requires an intermediate host, a freshwater snail of the genus Biomphalaria for its transmission. Given the limited options for treating Schistosoma mansoni infections in humans, much research has focused on developing methods to control transmission by its intermediate snail host. Biomphalaria glabrata. Comparative studies have shown that infection of the snail triggers complex cellular and humoral immune responses resulting in significant variations in parasite infectivity and snail susceptibility, known as the so-called polymorphism of compatibility. However, studies have mostly focused on characterizing the immunobiological mechanisms in sympatric interactions. Herein we used a combination of molecular and phenotypic approaches to compare the effect of infection in various sympatric and allopatric evolutionary contexts, allowing us to better understand the mechanisms of host-parasite local adaptation. Learning more about the immunobiological interactions between B. glabrata and S. mansoni could have important socioeconomic and public health impacts by changing the way we attempt to eradicate parasitic diseases and prevent or control schistosomiasis in the field.

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