Tick microbiome: the force within

Abstract

Ticks are obligate blood-feeders and serve as vectors of human and livestock pathogens worldwide. Defining the tick microbiome and deciphering the interactions between the tick and its symbiotic bacteria in the context of tick development and pathogen transmission will likely reveal new insights and spawn new paradigms to control tick-borne diseases. Descriptive observations on the tick microbiome that began almost a century ago serve as forerunners to the gathering momentum to define the tick microbiome in greater detail. This review will focus on the current efforts to address the microbiomes of diverse ticks, and the evolving understanding of tick microbiomes. There is hope that these efforts will bring a holistic understanding of pathogen transmission by ticks.

Keywords: tick endosymbionts; tick microbiome.

Figure 1. Predominant bacterial members of the tick microbiome

A schematic representation of bacterial genera frequently observed in the salivary glands (SG), midgut (MG), Ovary (Ov), and Malphigian tubules (Mp) of ticks. Arsenophonus species have been frequently identified in ticks, but the tissue distribution is not determined.

Figure 2. Changes in the microbial composition and the consequent immune responses in the tick gut

Alterations in the gut microbiome associated with feeding, development and infection could modulate the following immune response pathways in ticks: A. Toll pathway. Microbiota-induced activation of Spatzle, enabling Spatzle-Toll interaction and initiation of the signaling cascade resulting in the production of antimicrobial peptides (AMPs). B. Immunodeficiency (IMD) pathway. Sensing of Gram-negative peptidoglycan (Peptidoglycan) by the peptidoglycan recognition protein (PGRP-LC) to activate the signaling cascade leading to AMP production. C. Janus kinase/Signal transducer and activator of transcription JAK-STAT pathway. Microbiota and pathogen-induced activation of Dual oxidase (DUOX) results in the reactive oxygen species (ROS) production to control bacteria. ROS-mediated collateral damage to the gut epithelial cells initiates the release of cytokine-like molecule Unpaired 3 Upd that engages with its receptor, DOME, a signal transducing transmembrane protein receptor, to activate the JAK-STAT signaling pathway. STAT transcriptionally regulates pathways leading to immune responses, epithelial regeneration and repair, and peritrophic membrane integrity. AMPs and immune responses generated by Toll, IMD and JAK-STAT pathways influence pathogen survival, and also facilitate bacterial homeostasis (Based on citations , , and 89).