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Enteric Bacteria Counteract Lipopolysaccharide Induction of Antimicrobial Peptide Genes¹

Hans Lindmark^*, Karin C. Johansson^*, Svenja Stöven, Dan Hultmark, Ylva Engström and Kenneth Söderhäll^2,*

^* Department of Comparative Physiology, Evolutionary Biology Centre, Uppsala University, Uppsala, Sweden; Umeå Center for Molecular Pathogenesis, Umeå University, Umeå, Sweden; and Department of Molecular Biology and Functional Genomics, Stockholm University, Stockholm, Sweden

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, including E. coli, Salmonella typhimurium, Erwinia carotovora, and Pseudomonas aeruginosa, prevented LPS from inducing antimicrobial peptide genes, while Micrococcus luteus and Streptococcus equi did not. The inhibitory effect was seen at bacterial levels from 20 per mbn-2 cell, while antimicrobial peptides were induced at lower bacterial concentrations (2 bacteria per cell) also in the absence of added LPS. Gel shift experiment suggests that the inhibitory effect is upstream or at the level of the activation of the transcription factor Relish, a member of the NF-B/Rel family. The bacteria have to be in physical contact with the cells, but not phagocytosed, to prevent LPS induction. Interestingly, the inhibiting mechanism is, at least for E. coli, independent of the type III secretion system, indicating that the inhibitory mechanism is unrelated to the one earlier described for YopJ from Yersinia.

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