The humoral immunity of Drosophila involves the production of antimicrobial
peptides, which are induced by evolutionary conserved microbial molecules,
like LPS. By using Drosophila mbn-2 cells, we found that live bacteria, in
cluding E. coli, Salmonella typhimurium, Erwinia carotovora, and Pseudomona
s aeruginosa, prevented LPS from inducing antimicrobial peptide genes, whil
e Micrococcus luteus and Streptococcus equi did not. The inhibitory effect
was seen at bacterial levels from 20 per mbn-2 cell, while antimicrobial pe
ptides were induced at lower bacterial concentrations (less than or equal t
o2 bacteria per cell) also in the absence of added LPS. Gel shift experimen
t suggests that the inhibitory effect is upstream or at the level of the ac
tivation of the transcription factor Relish, a member of the NF-kappaB/Rel
family. The bacteria have to be in physical contact with the cells, but not
phagocytosed, to prevent LPS induction. Interestingly, the inhibiting mech
anism is, at least for E. coli, independent of the type III secretion syste
m, indicating that the inhibitory mechanism is unrelated to the one earlier
described for YopJ from Yersinia.