Dataset Information

Identifying sources of tick blood meals using unidentified tandem mass spectral libraries

ABSTRACT: Rapid and reliable identification of the vertebrate species on which a disease vector previously parasitized is imperative to study ecological factors that affect pathogen distribution and can aid the development of public health programs. We here describe a proteome profiling technique designed to identify the source of blood meals of hematophagous arthropods. This method employs direct spectral matching and thus does not require a priori knowledge of any genetic or protein sequence information. Using this technology, we can detect remnants of blood in blacklegged ticks (Ixodes scapularis) and correctly determine the vertebrate species from which the blood was derived even six months after the tick had fed. This biological fingerprinting methodology is sensitive, fast, cost-effective, and can potentially be adapted for other biological and medical applications when existing genome-based methods are impractical or ineffective.

INSTRUMENT(S): LCQ Classic

ORGANISM(S): Eryx Colubrinus Loveridgei Ixodes Scapularis (black-legged Tick) (deer Tick) Tamias Striatus (eastern Chipmunk) Rousettus Aegyptiacus (egyptian Rousette) (egyptian Fruit Bat) Sturnus Vulgaris (starling) Strix Varia (barred Owl) Malaclemys Terrapin (diamondback Terrapin) (testudo Terrapin) Pteropus Rodricensis (rodriguez Flying Fox) Sciurus Carolinensis (gray Squirrel) Panthera Leo (lion) Ovis Aries Corucia Zebrata Macropus Rufus (red Kangaroo) (megaleia Rufa) Alligator Mississippiensis (american Alligator) Colobus Guereza (mantled Guereza) (eastern Black-and-white Colobus Monkey) Chelodina Longicollis (snake-necked Turtle) (testudo Longicollis) Rhynchocyon Petersi (black And Rufous Elephant Shrew) Panthera Tigris (tiger) Nanger Dama Mhorr Equus Asinus Africanus Tremarctos Ornatus (spectacled Bear) Pituophis Melanoleucus (pine Snake) (coluber Melanoleucus) Peromyscus Leucopus (white-footed Mouse) Anas Platyrhynchos Capra Hircus (goat) Mus Musculus (mouse)

SUBMITTER: Wenguang Shao

PROVIDER: PXD000170 | Pride | 2014-04-03

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	README.txt	Txt
	filetospeciesmapping.txt	Txt
	onder_blood_source_tracking_unidentified_spectral_library.tgz	Other

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Publications

Identifying sources of tick blood meals using unidentified tandem mass spectral libraries.

Önder Özlem Ö Shao Wenguang W Kemps Brian D BD Lam Henry H Brisson Dustin D

Nature communications 20130101

Rapid and reliable identification of the vertebrate species on which a disease vector previously parasitized is imperative to study ecological factors that affect pathogen distribution and can aid the development of public health programs. Here we describe a proteome profiling technique designed to identify the source of blood meals of haematophagous arthropods. This method employs direct spectral matching and thus does not require a priori knowledge of any genetic or protein sequence informatio ...[more]

PMID: 23612287

Similar Datasets

Project description:Ticks are blood feeding arthropod ectoparasites that transmit pathogens, which cause diseases in humans and animals worldwide. In the past ten decades, the continuous human exploitation of environmental resources and the increase in human outdoor activities has promoted contact with arthropod vectors normally present in the wild, resulting in increased transmission of vector-borne pathogens. In addition, vector populations are expanding in response to climate change and human interventions that impact reservoir host movement and human exposure to infected vectors. Among these emerging vector-borne pathogens, Anaplasma phagocytophilum (Rickettsiales: Anaplasmataceae) has become an important tick-borne pathogen in the United States, Europe and Asia, with increasing numbers of infected people and animals every year. Diseases caused by A. phagocytophilum include human granulocytic anaplasmosis (HGA), equine and canine granulocytic anaplasmosis and tick-borne fever (TBF) in ruminants. The natural infection cycle of A. phagocytophilum is dependent upon the presence of infected vertebrate reservoir hosts and Ixodid tick vectors. In the United States and Europe the main vector species are Ixodes scapularis, Ixodes pacificus, and Ixodes ricinus, while a wide range of mammals, lizards, and birds serve as reservoir hosts for various A. phagocytophilum genotypes. A. phagocytophilum initially infects tick midgut cells and then subsequently develops in salivary glands for transmission to susceptible hosts during tick feeding where the pathogen infects granulocytic cells, primarily neutrophils. Anaplasma phagocytophilum develops within membrane-bound inclusions in the host cell cytoplasm. This pathogen has evolved with its tick and vertebrate hosts through dynamic processes involving genetic traits of the pathogen and hosts that collectively mediate pathogen infection, development, persistence, and survival. However, the mechanisms used by A. phagocytophilum for molecular mechanisms involved in tick-pathogen interactions have not been fully characterized. The objective of this study is to characterize the dynamics of the microRNA response in the tick vector Ixodes scapularis in response to A. phagocytophilum infection. To address this objective, the composition of tick microRNAs was characterize using RNA sequencing in I. scapularis tick cells in response to A. phagocytophilum infection. The discovery of these mechanisms provides evidence that a control strategy could be developed targeted at both vertebrate and tick hosts for more complete control of A. phagocytophilum and its associated diseases.

Project description:Introduction: Ixodes scapularis ticks are hematophagous arthropods capable of transmitting many infectious agents to humans. The process of blood feeding is an extended and continuous interplay between tick and host responses. While this process has been studied extensively in vitro, no global understanding of the host response to ticks has emerged. To address this issue, we measured skin-specific expression of 233 discrete genes at 8 time points during primary and secondary infestations of mice with pathogen-free I. scapularis nymphs. Selected results were then validated at the mRNA and protein levels. Results: Primary infestation was characterized by the late induction of an innate immune response. Lectin pattern recognition receptors, cytokines, and chemokines were upregulated consistent with increased neutrophil and macrophage migration. Gene ontology and pathway analyses of downregulated genes suggested inhibition of gene transcription and Th17 immunity. During the secondary infestation, additional genes were modulated suggesting a broader involvement of immune cells including CD8 and CD4 positive T lymphocytes. The cytokine response showed a mixed Th1/Th2 profile with a potential for T regulatory cell activity. Key gene ontology clusters observed during the secondary infestation were cell migration and activation. Matrix metalloproteinases were upregulated, apoptosis-related genes were differentially modulated, and immunoreceptor signaling molecules were upregulated. In contrast, transcripts related to mitogenic, WNT, Hedgehog, and stress pathways were downregulated. Conclusions: Our results support a model of tick feeding where lectin pattern recognition receptors orchestrate an innate inflammatory response during primary infestation that primes a mixed Th1/Th2 response upon secondary exposure. Tick feeding inhibits gene transcription and Th17 immunity. Salivary molecules may also inhibit upregulation of mitogenic, WNT, Hedgehog, and stress pathways and enhance the activity of T regulatory cells, production of IL-10, and suppressors of cytokine signaling molecules (SOCS). This study provides the first comprehensive transcriptional analysis of the host response at the tick bite site and suggests both a potential model of the host cutaneous response and candidate genes for further description and investigation. Ear biopsies from BALB/cJ mice infested with Ixodes scapularis nymphs were assayed at 12, 48, 72, and 96 hours after infestation during a primary and secondary exposure. 3 mice were measured at each time point. Controls were 3 similarly housed but tick-free mice.