Immunosuppression induced by entomopathogens is rescued by addition of apolipophorin III in the diamondback moth, Plutella xylostella

Apolipophorin III (ApoLpIII) has been known to play critical roles in lipid transport and immune activation in insects. This study reports a partial ApoLpIII gene cloned from the diamondback moth, Plutella xylostella. It showed that the gene was expressed in all developmental stages of P. xylostella. In larval stage, it was expressed in all tested tissues of hemocyte, fat body, gut, and epidermis. In response to bacterial challenge, the larvae showed an enhanced level of ApoLpIII expression by a quantitative real-time RT-PCR. RNA interference of ApoLpIII by its specific double stranded RNA (dsRNA) caused significant knockdown of its expression level and resulted in significant suppression in hemocyte nodule formation in response to bacterial challenge. However, larvae treated with the dsRNA exhibited a significant recovery in the cellular immune response by addition of a recombinant ApoLpIII. Parasitization by an endoparasitoid wasp, Cotesia plutellae, suppressed expression of ApoLpIII and resulted in a significant suppression in the hemocyte nodule formation. The addition of the recombinant ApoLpIII to the parasitized larvae significantly restored the hemocyte activity. Infection of an entomopathogenic bacterium, Xenorhabdus nematophila, caused potent pathogenicity of P. xylostella. However, the addition of the recombinant ApoLpIII to the infected larvae significantly prevented the lethal pathogenicity. This study suggests that ApoLpIII limits pathogenicity induced by parasitization or bacterial infection in P. xylostella.

ApoLpIII helps recognition of immune systems against pathogens. Infection by X. nematohila or C. plutellae inhibits ApoLpIII expression, which results in immunosuppression.Figure optionsDownload as PowerPoint slideResearch highlights
► Apolipophorin III (ApoLpIII) of Plutella xylostella showed an enhanced expression level in response to bacterial challenge.
► RNA interference of ApoLpIII caused significant knockdown of its expression level and resulted in significant suppression in hemocyte nodule formation in response to bacterial challenge.
► Parasitization by Cotesia plutellae or infection of Xenorhabdus nematophila suppressed expression of ApoLpIII and resulted in a significant suppression in the hemocyte nodule formation.
► The addition of the recombinant ApoLpIII to the parasitized larvae significantly restored the hemocyte activity.