Predator stress-induced immunosuppression: trade-off, immune redistribution or immune reconfiguration?

Abstract

Although predator exposure increases the risk of wound infections, it typically induces immunosuppression. A number of non-mutually exclusive hypotheses have been put forward to explain this immunosuppression, including: trade-offs between the immune system and other systems required for anti-predator behaviour, redistribution of immune resources towards mechanisms needed to defend against wound infections, and reconfiguration of the immune system to optimize defense under the physiological state of fight-or-flight readiness. We tested the ability of each hypothesis to explain the effects of chronic predator stress on the immune system of the caterpillar Manduca sexta. Predator stress induced defensive behaviours, reduced weight gain, increased development time and increased the concentration of the stress neurohormone octopamine. It had no significant effect on: hemocyte number, melanization rate, phenoloxidase activity, lysozyme-like activity, or nodule production. Predator stress reduced hemolymph glutathione concentrations. It also increased constitutive expression of the antimicrobial peptide attacin-1 but reduced attacin-1 expression in response to an immune challenge. These results best fit the immune reconfiguration hypothesis, although the other hypotheses are also consistent with some results. Interpreting stress related changes in immune function may require an examination at the level of the whole organism.