Colonization Resistance of Symbionts in Their Insect Hosts

Abstract

The symbiotic microbiome is critical in promoting insect resistance against colonization by exogenous microorganisms. The mechanisms by which symbionts contribute to the host's immune capacity is referred to as colonization resistance. Symbionts can protect insects from exogenous pathogens through a variety of mechanisms, including upregulating the expression of host immune-related genes, producing antimicrobial substances, and competitively excluding pathogens. Concordantly, insects have evolved fine-tuned regulatory mechanisms to avoid overactive immune responses against symbionts or specialized cells to harbor symbionts. Alternatively, some symbionts have evolved special adaptations, such as the formation of biofilms to increase their tolerance to host immune responses. Here, we provide a review of the mechanisms about colonization resistance of symbionts in their insect hosts. Adaptations of symbionts and their insect hosts that may maintain such symbiotic relationships, and the significance of such relationships in the coevolution of symbiotic systems are also discussed to provide insights into the in-depth study of the contribution of symbionts to host physiology and behavior.

Keywords: coevolution; colonization resistance; defensive symbiont; exogenous pathogen; insect.

Figure 1

Signaling network of the insect immune system to modulate AMP and ROS production in the midgut of Drosophila melanogaster in the presence of a low microbial load (A) and a high microbial load (B). Red lines and green lines indicate active pathways, where the green lines indicate activation and the red lines indicate inhibition. The thickness of the line indicates the strength of the signal. AMPs, antimicrobial peptides; Atf2, activating transcription factor 2; CanB, calcineurin B; Cad99c, cadherin 99c; DAP-PGN, diaminopimelic acid-type peptidoglycan; Duox, dual oxidase; Gαq, G protein αq subunit; GPCR, G-protein-coupled receptor; IKK, IκB kinase; IMD, immune deficiency; IP3, inositol 1,4,5-trisphosphate; MEKK1, MAPK and ERK kinase 1; MKK3, MAPK kinase 3; Mkp3, MAP kinase phosphatase-3; p38, p38 mitogen-activated protein kinase pathway; PGRPs, peptidoglycan recognition proteins; PIMS/Pirk, PGRP-LC-interacting inhibitors of IMD signaling; PKC, protein kinase C; PLCβ, phospholipase C-β; PM, peritrophic matrix; ROS, reactive oxygen species; TAK1, transforming growth factor-β-activated kinase 1.