Abstract
Upon entering the hemocoel of its insect host, the entomopathogenic nematode Heterorhabditis bacteriophora releases its symbiotic bacteria Photorhabdus luminescens, which is also a strong insect pathogen. P. luminescens is known to suppress the insect immune response independently following its release, but the nematode appears to enact its own immunosuppressive mechanisms during the earliest phases of an infection. H. bacteriophora was found to produce a unique set of excreted-secreted proteins in response to host hemolymph, and while basal secretions are immunogenic with regard to Diptericin expression through the Imd pathway, host-induced secretions suppress this expression to a level below that of controls in Drosophila melanogaster. This effect is consistent in adults, larvae, and isolated larval fat bodies, and the magnitude of suppression is dose-dependent. By reducing the expression of Diptericin, an antimicrobial peptide active against Gram-negative bacteria, the activated excreted-secreted products enable a more rapid propagation of P. luminescens that corresponds to more rapid host mortality. The identification and isolation of the specific proteins responsible for this suppression represents an exciting field of study with potential for enhancing the biocontrol of insect pests and treatment of diseases associated with excessive inflammation.
Highlights
The early steps of a Heterorhabditis bacteriophora infection are well-described with regard to the physical actions of the parasite
Exposure of Heterorhabditis bacteriophora Infective Juveniles (IJs) to Host Hemolymph Induces the Secretion of Unique Proteins
To investigate the proteins secreted in response to host stimulus, groups of 200, 100, or 25 thousand (k) H. bacteriophora IJs were activated as previously described [11]
Summary
The early steps of a Heterorhabditis bacteriophora infection are well-described with regard to the physical actions of the parasite. Upon migration to a host, the majority of the infective juveniles (IJ) enter the insect through natural openings, the IJ can generate tears in the intersegmental membrane to gain entry [1]. Once the parasite enters the hemocoel environment, the nematode slowly releases, following a 30-min lag time, the bacterial endosymbiont Photorhabdus luminescens that it maintains as a secondary phase in its gut [2]. The degree of melanization and encapsulation of the IJ has been shown to correlate to the survival of the insect [7], so the nematode must to some degree fare for itself in terms of immune suppression during the early phase of an infection. Heterorhabditis has a vested interest in promoting Photorhabdus survival, so some early IJ-based immune suppression may be targeted toward developing a more hospitable hemolymph environment for its symbiont
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