Abstract
Ixodid ticks transmit various pathogens of deadly diseases to humans and animals. However, the specific molecule that functions in the recognition and control of pathogens inside ticks is not yet to be identified. Class B scavenger receptor CD36 (SRB) participates in internalization of apoptotic cells, certain bacterial and fungal pathogens, and modified low-density lipoproteins. Recently, we have reported on recombinant HlSRB, a 50-kDa protein with one hydrophobic SRB domain from the hard tick, Haemaphysalis longicornis. Here, we show that HlSRB plays vital roles in granulocyte-mediated phagocytosis to invading Escherichia coli and contributes to the first-line host defense against various pathogens. Data clearly revealed that granulocytes that up-regulated the expression of cell surface HlSRB are almost exclusively involved in hemocyte-mediated phagocytosis for E. coli in ticks, and post-transcriptional silencing of the HlSRB-specific gene ablated the granulocytes' ability to phagocytose E. coli and resulted in the mortality of ticks due to high bacteremia. This is the first report demonstrating that a scavenger receptor molecule contributes to hemocyte-mediated phagocytosis against exogenous pathogens, isolated and characterized from hematophagous arthropods.
Highlights
The ixodid ticks (Arthropoda: Ixodidae), popularly known as hard ticks, serve as a unique vector of various pathogens that cause deadly diseases, such as Lyme disease, tick-borne encephalitis, Rocky Mountain spotted fever, babesiosis, theileriosis, and anaplasmosis, during hematophagy
The current observations were performed on plasmatocytes and granulocytes of female H. longicornis ticks (Fig. 1A), since they are generally recognized as a predominant class of phagocytes circulating in hemolymph of ticks [6,21,22,23]
The survival rates of RNAi-ticks 18, 24, and 30 hours after E. coli injection were 64.1%, 22.5%, and 0%, respectively (Fig. 4), indicating a marked decrease with time. These results indicated that almost all UF and partially fed (PF) ticks could survive after proper control of invaded E. coli but RNAi-ticks had to succumb to E. coli burdens mainly due to the recognition failure in pathogenassociated molecular patterns (PAMPs) [4,27] caused by infection due to high bacteremia
Summary
The ixodid ticks (Arthropoda: Ixodidae), popularly known as hard ticks, serve as a unique vector of various pathogens that cause deadly diseases, such as Lyme disease, tick-borne encephalitis, Rocky Mountain spotted fever, babesiosis, theileriosis, and anaplasmosis, during hematophagy. Ticks are only second to mosquitoes as vectors of various pathogens that cause deadly diseases of human and animals [1]. It is of current interest to look at the molecular scenario, in particular, the role of scavenger receptor in hemocyte-mediated phagocytosis, inside vector ticks, which play an important role in first-line host defense against invading pathogens. Phagocytosis in mammals is mainly achieved by mononuclear phagocytic cells, such as macrophages and dendritic cells and polynuclear neutrophils [3]. In arthropods, such as insects [4] and ticks [5,6], phagocytosis is achieved mainly by the circulating plasmatocytes and/or granulocytes, in the hemolymph. The molecular mechanisms of hemocyte-mediated phagocytosis in arthropods have not been intensively investigated [4]
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