The above describes work, and speculation, about bacterial mechanisms of surviving host anti-microbial defences. For symbionts that are beneficial, the host also carries an interest in the maintenance of the symbiont. While not seen in some cases (e.g. Riesia is not ignored by the host systems when extracellular), there is some evidence of it in others, notably the SZPE-weevil interaction. As discussed above, this bacterium moves from bacteriome into the haemolymph during nymphal maturation. In this system, bacteriome tissue expresses a peptidoglycan-recognition protein long chain B (PGRP-LB) homologue. PGRP-LB homologues in Drosophila have the ability to cleave peptidoglycan, reducing exposure to the bacterial elicitors of immune cascades that would potentially cause harm to primary symbionts. Interestingly, this gene is particularly strongly expressed at the time when bacterial release occurs (Anselme et al., 2006). An interpretation of this is that the host is actively upregulating an enzyme that removes elicitors of humoral immunity, and acting prophy-latically to prevent immune response from prior infections from killing off the beneficial symbiont. A prediction of this hypothesis is that the weevil will be more prone to opportunistic pathogens in this phase.
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