Ticks are notorious ectoparasites that exclusively feed on host's blood for a period of 10 days or longer. On blood-feeding, an adult female tick gains 100-200 times increased body weight compared to its prefeeding stage. Despite the host's armoury of rejection mechanisms, ticks manage to remain attached until a full blood-meal is ensured. The molecular machineries that make the tick a success with its feeding, however, remain to date unknown. We demonstrate that the Kunitz-like protein, Haemangin, identified from the salivary glands of the tick Haemaphysalis longicornis, plays vital roles in blood-feeding success. Using both cell- and chick embryo-based bioassays, we have shown that Haemangin efficiently disrupted angiogenesis and wound healing processes. Our biochemical data strongly support such a role. Together, these favor ticks to remain attached and allow persistent feeding. Additionally, in a rabbit model, we reveal that an elevated expression of Haemangin is associated with acquisition of full blood-meals. Haemangin-knockdown ticks fail to prevent angiogenesis in host's tissues and consequently achieve only a poor blood-meal as compared to normal ticks. We conclude that Haemangin is vital for tick's survival and can be a novel therapeutic target against ticks and tick-borne diseases, including tumor angiogenesis.
(Research Team for Zoonosis, TEL +81-29-838-7708)
Reference:
Islam, MK. et al. (2009) PLoS Pathog. 5:e1000497.
