Milder winters contribute to changes in wildlife-host populations, as well as shortening of the previously naturally occurring breaks in tick activity, resulting in a consistent increase in tick bite–associated (TB-associated) health complications annually ( 2). Steadily increasing tick prevalence has been reported globally in recent years, a trend that is predicted to increase with the rise in global temperatures and consequently more temperate climate ( 1).
#FEEDY SKIN SKIN#
Ticks are hematophagous ectoparasites, with the skin representing the main interface of host-vector interaction that may become the site of tick-borne pathogen transmission. Collectively, we showed that tick feeding exerts profound changes on the skin immune network that interfere with the primary response against tick-borne pathogens. Preincubation of spirochetes with tick salivary gland extracts hampered accumulation of immune cells and increased spirochete loads. In early stages of Borrelia burgdorferi model infections, we detected strain-specific immune responses and close spatial relationships between macrophages and spirochetes. T cells upregulated tissue residency markers, while lymphocytic cytokine production was impaired. Following tick attachment, we observed rapidly occurring patterns of immunomodulation, including increases in neutrophils and cutaneous B and T cells. Here, we assessed human skin and blood samples upon tick bite and developed a human skin explant model mimicking Ixodes ricinus bites and tick-borne pathogen infection. However, the immunological consequences of tick feeding for human skin remain unclear. During cutaneous tick attachment, the feeding cavity becomes a site of transmission for tick salivary compounds and tick-borne pathogens.
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