It was recently observed that a glucose-enriched diet activates the insulin-like pathway in Caenorhabditis elegans, resulting in an inhibition of the FOXO transcription factor DAF-16. Because this signalling pathway is highly conserved from invertebrates to mammals and DAF-16 is a key player in innate immunity, we wondered whether a high-glucose diet, resembling the hyperglycaemic conditions in diabetic patients, would affect the susceptibility of C. elegans to bacterial pathogens isolated from different clinical situations (urinary tract or diabetic foot infections). We confirmed previous reports showing that such a diet decreases the lifespan of C. elegans fed with an avirulent Escherichia coli strain. However, glucose-fed nematodes appeared to be more resistant to most clinical isolates tested, showing that this invertebrate model does not mimic infections encountered in human diabetes, where patients show increased susceptibility to bacterial infections. This study also suggests that modulation of innate immunity in C. elegans, upon activation of the IGF1/insulin-like pathway by glucose, is not exclusively mediated by DAF-16, but also involves an additional factor that requires DAF-16 activity.