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Adiponectin inhibits acquisition of the Lyme disease agent by ticks [Tick]

ABSTRACT: Tick gut and salivary gland global gene expression change after feeding on adiponectin wildtype and knockout mice

ORGANISM(S): Ixodes scapularis

PROVIDER: GSE233660 | GEO | 2024/05/01

REPOSITORIES: GEO

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Adiponectin inhibits acquisition of the Lyme disease agent by ticks [Tick]

Project description:Adiponectin inhibits acquisition of the Lyme disease agent by ticks [Tick]

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Adiponectin in the mammalian host influences ticks' acquisition of the Lyme disease pathogen Borrelia

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Tick Adiponectin Receptor-Mediated Phospholipid Metabolism Contributes to Borrelia burgdorferi Colonization

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Project description:Arthropod-borne pathogens cause some of the most important human and animal infectious diseases. Many vectors acquire or transmit pathogens through the process of blood feeding. Here, we report adiponectin, the most abundant adipocyte-derived hormone circulating in human blood, directly or indirectly inhibits acquisition of the Lyme disease agent, Borrelia burgdorferi, by Ixodes scapularis ticks. Rather than altering tick feeding or spirochete viability, adiponectin or its associated factors induces host histamine release when the tick feeds, which leads to vascular leakage, infiltration of neutrophils and macrophages, and inflammation at the bite site. Consistent with this, adiponectin-deficient mice have diminished pro-inflammatory responses, including interleukin (IL)-12 and IL-1β, following a tick bite, compared with wild-type animals. All these factors mediated by adiponectin or associated factors influence B. burgdorferi survival at the tick bite site. These results suggest a host adipocyte-derived hormone modulates pathogen acquisition by a blood-feeding arthropod.

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Tick Adiponectin Receptor-Mediated Phospholipid Metabolism Contributes to Borrelia burgdorferi Colonization

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