Abstract
Ticks are hematophagous arachnids transmitting a wide variety of pathogens including viruses, bacteria, and protozoans to their vertebrate hosts. The tick vector competence has to be intimately linked to the ability of transmitted pathogens to evade tick defense mechanisms encountered on their route through the tick body comprising midgut, hemolymph, salivary glands or ovaries. Tick innate immunity is, like in other invertebrates, based on an orchestrated action of humoral and cellular immune responses. The direct antimicrobial defense in ticks is accomplished by a variety of small molecules such as defensins, lysozymes or by tick-specific antimicrobial compounds such as microplusin/hebraein or 5.3-kDa family proteins. Phagocytosis of the invading microbes by tick hemocytes is likely mediated by the primordial complement-like system composed of thioester-containing proteins, fibrinogen-related lectins and convertase-like factors. Moreover, an important role in survival of the ingested microbes seems to be played by host proteins and redox balance maintenance in the tick midgut. Here, we summarize recent knowledge about the major components of tick immune system and focus on their interaction with the relevant tick-transmitted pathogens, represented by spirochetes (Borrelia), rickettsiae (Anaplasma), and protozoans (Babesia). Availability of the tick genomic database and feasibility of functional genomics based on RNA interference greatly contribute to the understanding of molecular and cellular interplay at the tick-pathogen interface and may provide new targets for blocking the transmission of tick pathogens.
Highlights
Ondrej Hajdušek 1, Radek Šíma1, Nieves Ayllón 2, Marie Jalovecká 3,4, Jan Perner 3, José de la Fuente 2,5 and Petr Kopácek1*
The success rate of pathogens transmitted by ticks is mainly given by the favorable aspects of tick physiology arising from their adaptation to the relatively long-lasting blood feeding
It was demonstrated that the 5.3-kDa family members were markedly upregulated in the salivary glands and hemocytes during A. phagocytophilum infection and were involved in the I. scapularis defense against this pathogen. They were shown to be effector molecules regulated by the JAKSTAT pathway (Liu et al, 2012) and the I. scapularis genome contains components of the putative Toll and Imd immune signaling pathways (Megy et al, 2012; Severo et al, 2013), the 5.3-kDa family regulation by Janus kinase (JAK)/Signal transducer and activator of transcription (STAT) is the only so far described case of tick antimicrobial response controlled by a signaling pathway
Summary
Ondrej Hajdušek 1, Radek Šíma, Nieves Ayllón 2, Marie Jalovecká 3,4, Jan Perner 3, José de la Fuente 2,5 and Petr Kopácek1*. Tick-pathogen interface is difference in the time of transmission between the Borrelia spirochetes causing Lyme disease (transmission several days after attachment) and relapsing fever (transmission several minutes after attachment) vectored by the hard and soft ticks, respectively (Sonenshine, 1991) Another important aspect that should be taken into consideration is the tick feeding strategy, the differences between one- and multi-host ticks in terms of transovarial and transstadial transmission. The transmitting pathogen acquired from the infected host has to overcome several tissue barriers within the tick body comprising midgut, hemocoel and salivary glands or ovary (in case of transovarial transmission) Each of these compartments may play a decisive role in the tick vector competence for a certain microbe. The general features of tick immunity will be further discussed in relation to our current knowledge of tick interaction with the three most intensively studied agents of tick-borne diseases, represented here by Borrelia spirochete, intracellular rickettsia Anaplasma, and malaria-like protozoa Babesia
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