Receptor for advanced glycation end-product (RAGE) modulates
inflammation during feeding of tick, Haemaphysalis longicor
Abstract
Abstract Ticks are notorious blood-sucking ectoparasites
affecting both humans and animals, and serve as a unique vector of
various deadly diseases. Here, we have shown the roles of the receptor
for advanced glycation end-products (RAGE) during repeated infestations
by the tick, Haemaphysalis longicornis using
RAGE-/- mice. In primary infestation, a large
blood pool developed which was flooded with numerous RBC, especially
during the rapid feeding phase of the tick both in wild type (wt) and
RAGE-/- mice. Very few inflammatory cells were
detected around the zones of hemorrhage in the primary infestations.
However, number of inflammatory cells gradually increased in the
subsequent tick infestations and at the 3 rd
infestations number of inflammatory cells reached to the highest level
(350.3±16.8 cells/focus), and the site of attachment was totally
occupied by the inflammatory cells in wild type (wt) mice whereas very
few cells were detected at the ticks’ biting sites in
RAGE-/- mice. RAGE was highly expressed in the
3 rd infestation in wt mice. In the 3
rd infestation, infiltration of innate lymphoid cells
type 2 (ILC2s), expression of S100A8 and S100B significantly increased
at the biting sites of ticks in wt, but not in RAGE
-/- mice. Also, peripheral eosinophil counts
significantly increased in wt but not in RAGE
-/- mice. Taken together, our study revealed that
RAGE-mediated inflammation and eosinophils played crucial roles in the
tick induced inflammatory reactions.