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Enteric bacteria counteract lipopolysaccharide induction of antimicrobial peptide genes.
Umeå universitet, Medicinsk fakultet, Umeå centrum för molekylär patogenes (UCMP) (Medicinska fakulteten). Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi. Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi, Klinisk bakteriologi. (Dan Hultmark)
Umeå universitet, Medicinsk fakultet, Umeå centrum för molekylär patogenes (UCMP) (Medicinska fakulteten). (Dan Hultmark)
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2001 (Engelska)Ingår i: J Immunol, ISSN 0022-1767, Vol. 167, nr 12, s. 6920-3Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

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 (< or =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-kappaB/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.

Ort, förlag, år, upplaga, sidor
2001. Vol. 167, nr 12, s. 6920-3
Nyckelord [en]
Animals, Antimicrobial Cationic Peptides/*biosynthesis/genetics, Cell Line, Digestive System/*microbiology, Down-Regulation, Drosophila Proteins/*biosynthesis/genetics, Drosophila melanogaster/genetics/*immunology/metabolism, Electrophoretic Mobility Shift Assay, Escherichia coli/pathogenicity, Kinetics, Lipopolysaccharides/*antagonists & inhibitors, Phagocytosis, RNA; Messenger/biosynthesis, Species Specificity, Transcription Factors/metabolism, Transcription; Genetic
Identifikatorer
URN: urn:nbn:se:umu:diva-17064PubMedID: 11739510OAI: oai:DiVA.org:umu-17064DiVA, id: diva2:156737
Tillgänglig från: 2007-10-28 Skapad: 2007-10-28 Senast uppdaterad: 2018-06-09Bibliografiskt granskad

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Stöven, SvenjaHultmark, Dan

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