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Background  Pathogens can infect their hosts through different routes. For studying the consequences for host resistance, we here used the entomopathogen  Bacillus thuringiensis  and the red flour beetle  Tribolium castaneum  for oral and systemic (i. e. pricking the cuticle) experimental infection. In order to characterize the molecular mechanisms underpinning the two different infection routes, the transcriptomes of beetles of two different  T. castaneum  populations – one recently collected population (Cro1) and a commonly used laboratory strain (SB) – were analyzed using a next generation RNA sequencing approach.    Results  The genetically more diverse population Cro1 showed a significantly larger number of differentially expressed genes. While both populations exhibited similar reactions to pricking, their expression patterns in response to oral infection differed remarkably. In particular, the Cro1 population showed a strong response of cuticular proteins and developmental genes, which might indicate an adaptive developmental flexibility that was lost in the SB population presumably as a result of inbreeding. The immune response of SB was primarily based on antimicrobial peptides, while Cro1 relied on responses mediated by phenoloxidase and reactive oxygen species, which may explain the higher resistance of this strain against oral infection.    Conclusions  Our data demonstrate that immunological and physiological processes underpinning the two different routes of infection are clearly distinct, and that host populations particularly differ in responses to oral infection. Furthermore, gene expression upon pricking infection entailed a strong signal of wounding, highlighting the importance of pricking controls in future infection studies.    Electronic supplementary material  The online version of this article (doi:10.1186/1471-2164-15-445) contains supplementary material, which is available to authorized users.

Infection routes matter in population-specific responses of the red flour beetle to the entomopathogen Bacillus thuringiensis