Ticks: More Than Just a Pathogen Delivery Service

Park, Jason M.; Chávez, Adela S. Oliva; Shaw, Dana K.

doi:10.3389/fcimb.2021.739419

Cited by 9 publications

(8 citation statements)

References 106 publications

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“…During this period, the ticks secrete a diverse range of bioactive molecules to modulate host responses in order to achieve feeding success and survival [ 11 ]. This complex range of secreted protein and non-protein tick salivary molecules has been reviewed elsewhere [ 12 ]. Some of the host processes that are known to be disrupted by the hematophagy of cattle ticks include blood coagulation, cytokine secretion, cell adhesion, as well as leukocyte recruitment to the feeding site.…”

Section: Introductionmentioning

confidence: 99%

Transcriptional changes in the peripheral blood leukocytes from Brangus cattle before and after tick challenge with Rhipicephalus australis

et al. 2022

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Background Disease emergence and production loss caused by cattle tick infestations have focused attention on genetic selection strategies to breed beef cattle with increased tick resistance. However, the mechanisms behind host responses to tick infestation have not been fully characterised. Hence, this study examined gene expression profiles of peripheral blood leukocytes from tick-naive Brangus steers (Bos taurus x Bos indicus) at 0, 3, and 12 weeks following artificial tick challenge experiments with Rhipicephalus australis larvae. The aim of the study was to investigate the effect of tick infestation on host leukocyte response to explore genes associated with the expression of high and low host resistance to ticks. Results Animals with high (HR, n = 5) and low (LR, n = 5) host resistance were identified after repeated tick challenge. A total of 3644 unique differentially expressed genes (FDR < 0.05) were identified in the comparison of tick-exposed (both HR and LR) and tick-naive steers for the 3-week and 12-week infestation period. Enrichment analyses showed genes were involved in leukocyte chemotaxis, coagulation, and inflammatory response. The IL-17 signalling, and cytokine-cytokine interactions pathways appeared to be relevant in protection and immunopathology to tick challenge. Comparison of HR and LR phenotypes at timepoints of weeks 0, 3, and 12 showed there were 69, 8, and 4 differentially expressed genes, respectively. Most of these genes were related to immune, tissue remodelling, and angiogenesis functions, suggesting this is relevant in the development of resistance or susceptibility to tick challenge. Conclusions This study showed the effect of tick infestation on Brangus cattle with variable phenotypes of host resistance to R. australis ticks. Steers responded to infestation by expressing leukocyte genes related to chemotaxis, cytokine secretion, and inflammatory response. The altered expression of genes from the bovine MHC complex in highly resistant animals at pre- and post- infestation stages also supports the relevance of this genomic region for disease resilience. Overall, this study offers a resource of leukocyte gene expression data on matched tick-naive and tick-infested steers relevant for the improvement of tick resistance in composite cattle.

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Section: Introductionmentioning

confidence: 99%

Transcriptional changes in the peripheral blood leukocytes from Brangus cattle before and after tick challenge with Rhipicephalus australis

et al. 2022

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“…For example, vector-borne microbes must adapt and survive in both vertebrate hosts and arthropod vectors (2). These two environments differ significantly with discrepancies in body temperature, nutrient availability, cell types infected, physiological architecture, and immunological pressures (2). Most of our understanding of tick-borne pathogens focuses on interactions with mammalian hosts, as this is where disease occurs.…”

Section: Introductionmentioning

confidence: 99%

“…In contrast, little is known about how tick-vectored pathogens mediate interactions with the arthropod. With over 680 million years of evolution separating ticks from mammals (3), our understanding of mammal-pathogen interactions cannot simply be transposed onto ticks (2).…”

Section: Introductionmentioning

confidence: 99%

“…Multi-host pathogens often have specific adaptation mechanisms to survive in disparate environments (1). For example, vector-borne microbes must adapt and survive in both vertebrate hosts and arthropod vectors (2). These two environments differ significantly with discrepancies in body temperature, nutrient availability, cell types infected, physiological architecture, and immunological pressures (2).…”

Section: Introductionmentioning

confidence: 99%

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AnAnaplasma phagocytophilumT4SS effector, AteA, is essential for tick infection

Park

Genera

Fahy

et al. 2023

Preprint

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Pathogens must adapt to disparate environments in permissive host species, a feat that is especially pronounced for vector-borne microbes, which transition between vertebrate hosts and arthropod vectors to complete their lifecycles. Most knowledge about arthropod-vectored bacterial pathogens centers on their life in the mammalian host, where disease occurs. However, disease outbreaks are driven by the arthropod vectors. Adapting to the arthropod is critical for obligate intracellular rickettsial pathogens, as they depend on eukaryotic cells for survival. To manipulate the intracellular environment, these bacteria use Type IV Secretion Systems (T4SS) to deliver effectors into the host cell. To date, few rickettsial T4SS translocated effectors have been identified and have only been examined in the context of mammalian infection. We identified an effector from the tick-borne rickettsial pathogenAnaplasma phagocytophilum, HGE1_02492, as critical for survival in tick cells and acquisition by ticks in vivo. Conversely, HGE1_02492 was dispensable during mammalian cell culture and murine infection. We show HGE1_02492 is translocatable in a T4SS-dependent manner to the host cell cytosol. In eukaryotic cells, the HGE1_02492 localized with cortical actin filaments, which is dependent on multiple sub-domains of the protein. HGE1_02492 is the first arthropod-vector specific T4SS translocated effector identified from a rickettsial pathogen. Moreover, the subcellular target of HGE1_02492 suggests thatA. phagocytophilumis manipulating actin to enable arthropod colonization. Based on these findings, we propose the name AteA forAnaplasma(phagocytophilum) tick effector A. Altogether, we show thatA. phagocytophilumuses distinct strategies to cycle between mammals and arthropods.

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“…Ticks are prolific spreaders of pathogens that plague human and animal health including bacteria, viruses, and protozoan parasites [1][2][3][4] . A crucial phase in the tick-borne pathogen lifecycle is the time spent colonizing and persisting within the arthropod vector 5 . While many forces impact the way transmissible pathogens interface with their arthropod vectors, recent advances have demonstrated that tick immunity is an important influence shaping this interaction.…”

Section: Introductionmentioning

confidence: 99%

PERK-mediated antioxidant response is key for pathogen persistence in ticks

Rosche,

Hurtado,

Fisk

et al. 2023

Preprint

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A crucial phase in the lifecycle of tick-borne pathogens is the time spent colonizing and persisting within the arthropod. Tick immunity is emerging as a key force shaping how transmissible pathogens interact with the vector. How pathogens remain in the tick despite immunological pressure remains unknown. In persistently infected Ixodes scapularis, we found that Borrelia burgdorferi (Lyme disease) and Anaplasma phagocytophilum (granulocytic anaplasmosis) activate a cellular stress pathway mediated by the endoplasmic reticulum receptor PERK and the central regulatory molecule, eIF2α. Disabling the PERK pathway through pharmacological inhibition and RNAi significantly decreased microbial numbers. In vivo RNA interference of the PERK pathway not only reduced the number of A. phagocytophilum and B. burgdorferi colonizing larvae after a bloodmeal, but also significantly reduced the number of bacteria that survive the molt. An investigation into PERK pathway-regulated targets revealed that A. phagocytophilum and B. burgdorferi induce activity of the antioxidant response regulator, Nrf2. Tick cells deficient for nrf2 expression or PERK signaling showed accumulation of reactive oxygen and nitrogen species in addition to reduced microbial survival. Supplementation with antioxidants rescued the microbicidal phenotype caused by blocking the PERK pathway. Altogether, our study demonstrates that the Ixodes PERK pathway is activated by transmissible microbes and facilitates persistence in the arthropod by potentiating an Nrf2-regulated antioxidant environment.

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Ticks: More Than Just a Pathogen Delivery Service

Cited by 9 publications

References 106 publications

Transcriptional changes in the peripheral blood leukocytes from Brangus cattle before and after tick challenge with Rhipicephalus australis

Transcriptional changes in the peripheral blood leukocytes from Brangus cattle before and after tick challenge with Rhipicephalus australis

AnAnaplasma phagocytophilumT4SS effector, AteA, is essential for tick infection

PERK-mediated antioxidant response is key for pathogen persistence in ticks

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