Abstract

Abstract Ticks are obligate haematophagous ectoparasites of animals and humans. In the livestock industry, economic losses due to ticks and tick borne diseases (TBD) amount to million of dollars. In public health, ticks are second to mosquitoes in terms of impact of human diseases. CDC has listed 14 TBD causative agents of which, 9 are transmitted by Amblyomma americanum and Ixodes scapularis. With few exceptions, the transmission of TBD agents requires successful tick feeding. Thus understanding tick-feeding mechanism is a critical step in developing novel methods to stop TBD agent transmission. We know that ticks secrete numerous tick saliva proteins that suppress host immunity to facilitate feeding and disease agent colonization. However, mechanisms of how the tick suppresses host immunity remain unanswered. We investigated the effect of 15 A. americanum and I. scapularis recombinant tick saliva proteins (rTSPs) on murine macrophage function as revealed by expression of pro-inflammatory co-stimulatory markers (CD40, C80, and CD86). Additionally, the effect of rTSP on macrophage secretion of pro- and anti-inflammatory cytokines (TNFa, IL1, IL6, IL-10, TGF beta) was also investigated. Our analysis identified five pro-inflammatory and two anti-inflammatory tick saliva proteins. The two anti-inflammatory proteins appear to reverse the expression of co-stimulatory markers activated by LPS and rTSPs. These data collectively demonstrate the presence of a “bait and switch” mechanism through which the tick may evade host immunity. We propose that ticks secrete two types of immune-modulating proteins: those that stimulate host immune cells and those that dampen the activated cells.

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