When injected with Escherichia coli, the insect system of cellular and humoral immunity is upregu-lated, and the invading bacteria are killed through phagocytosis, nodulation, and the expression of antimicrobial peptides (AMPs). Removal of elements of this system (e.g. mutations that disrupt the cascade leading to AMPs) is accompanied by sepsis and death in response to challenge. As argued in Chapters 2 and 6 in this volume, the insect innate immune system is a formidable system for protection against natural enemies. Notwithstanding this, insects possess a complex flora of bacterial symbionts. Parasitic symbionts must either not induce cellular and humoral responses, or, if they do induce it, survive this induction. As close antagonists, they may co-evolve with host systems in arms races. Primary symbionts, and secondary symbionts that induce resistance to natural enemies or confer ecological adaptation to host plants, differ from this in that both host and bacteria have an interest in the persistence of the bacteria, and their transmission to the next generation. The systems of destruction that are normally induced by bacterial presence must either not be invoked by the bacteria, or not affect them significantly.
The explanation for symbiont survival in a hostile host has largely relied on the intracellular location of many of these agents. We first discuss why this may matter, and whether the view of the intracellular location is a fair one. We then discuss whether the absence of response to intracellular bacteria is sufficient to make ignorable for the purpose of interaction with the immune system.
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