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- W4313366359 abstract "Abstract Vector-borne diseases pose significant global health concerns with tick-borne disease doubling over the past 13 years. Tick-borne ehrlichiosis are life-threatening diseases that affect humans and animals. Many studies have been focused on the pathogenesis of these infections; however not much is known about in vivo immune responses to tick transmitted ehrlichiosis. With our model of a human pathogen Ehrlichia (EML) transmitted by ticks, we observed intense changes at the site of infection that persisted for several days. Lethal infection suggests an involvement of vascular dysfunction in disease pathogenesis. Therefore, the goal of this study was to evaluate the granulocyte response to tick transmission, primarily eosinophils. Skin site of the arthropod attachment showed intense infiltration of granulocytes, extending through dermal and subcutaneous tissue. The predominant cells contained eosinophilic granules and were surrounded by other poly and mono-nuclear cells. Also, we further identified increased cellular signaling associated with granulocyte recruitment and vascular dysfunction. The progression of disease was also characterized by increased eosinophils in the blood and immune mediators (e.g. IL-1β) in serum, indicative of proliferation, chemotaxis, and activation of these cells. A needle infection model demonstrated that granulocytes were implicated in immunopathology, bacterial replication, over-production of cytokines/chemokines. We believe that tick transmitted ehrlichiosis induces eosinophilic inflammation that result in release of an arsenal of mediators that regulate inflammation and vascular permeability and could be involved in the establishment of infection and/or disease development." @default.
- W4313366359 created "2023-01-06" @default.
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- W4313366359 date "2019-05-01" @default.
- W4313366359 modified "2023-09-26" @default.
- W4313366359 title "Eosinophils in tick transmitted ehrlichial infection" @default.
- W4313366359 doi "https://doi.org/10.4049/jimmunol.202.supp.190.58" @default.
- W4313366359 hasPublicationYear "2019" @default.
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