Journal
ENTOMOLOGIA EXPERIMENTALIS ET APPLICATA
Volume 146, Issue 3, Pages 321-331Publisher
WILEY
DOI: 10.1111/eea.12032
Keywords
chemical defense; acquired plant metabolite; immune defense; Lepidoptera; Solanaceae; Sphingidae; Nicotiana attenuata; tobacco hornworm; Enterococcus faecalis; Pseudomonas aeruginosa; chlorogenic acid
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Funding
- National Institutes of Health [R01-AI083932]
- National Science Foundation [IOB-0950225]
- Ford Foundation
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [0950225] Funding Source: National Science Foundation
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Plant phenolics are generally thought to play significant roles in plant defense against herbivores and pathogens. Many plant taxa, including Solanaceae, are rich in phenolic compounds and some insect herbivores have been shown to acquire phenolics from their hosts to use them as protection against their natural enemies. Here, we demonstrate that larvae of an insect specialist on Solanaceae, the tobacco hornworm, Manduca sexta L. (Lepidoptera: Sphingidae), acquire the plant phenolic chlorogenic acid (CA), and other caffeic acid derivatives as they feed on one of their hosts, Nicotiana attenuata L. (Solanaceae), and on artificial diet supplemented with CA. We test the hypothesis that larvae fed on CA-supplemented diet would have better resistance against bacterial infection than larvae fed on a standard CA-free diet by injecting bacteria into the hemocoel of fourth instars. Larvae fed CA-supplemented diet show significantly higher survival of infection with Enterococcus faecalis (Andrewes & Horder) Schleifer & Kilpper-Balz, but not of infection with the more virulent Pseudomonas aeruginosa (Schroeter) Migula. Larvae fed on CA-supplemented diet possess a constitutively higher number of circulating hemocytes than larvae fed on the standard diet, but we found no other evidence of increased immune system activity, nor were larvae fed on CA-supplemented diet better able to suppress bacterial proliferation early in the infection. Thus, our data suggest an additional defensive function of CA to the direct toxic inhibition of pathogen proliferation in the gut.
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