The Role of Potassium in Inflammasome Activation by Bacteria*
| Autor: | Olaf Gross, Thomas J. Evans, Virginie Pétrilli, Cecilia S. Lindestam Arlehamn, Jürg Tschopp |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2010 |
| Předmět: |
Salmonella typhimurium
Immunology Immunology/Innate Immunity Immunoblotting Interleukin-1beta Caspase 1 NLR Proteins Animals Bacterial Proteins/metabolism Caspase 1/metabolism Inflammation/immunology Inflammation/metabolism Interleukin-1beta/metabolism Mice Mice Inbred C57BL Potassium/metabolism Pseudomonas Infections/immunology Pseudomonas Infections/metabolism Pseudomonas aeruginosa/pathogenicity Salmonella Infections/immunology Salmonella Infections/metabolism Salmonella typhimurium/pathogenicity Cytokines/Interleukins Biochemistry Inflammasome Cell membrane 03 medical and health sciences 0302 clinical medicine Bacterial Proteins NLRC4 medicine Extracellular Secretion Cytokines/Induction Pseudomonas Infections Molecular Biology 030304 developmental biology Inflammation 0303 health sciences biology Organisms/Bacteria Proteases/Caspase Cell Biology medicine.anatomical_structure Pseudomonas aeruginosa Salmonella Infections biology.protein Biophysics Potassium Flagellin Intracellular 030215 immunology medicine.drug |
| Zdroj: | The Journal of Biological Chemistry Journal of Biological Chemistry, vol. 285, no. 14, pp. 10508-10518 |
| ISSN: | 1083-351X 0021-9258 |
| Popis: | Many Gram-negative bacteria possess a type III secretion system (TTSS( paragraph sign)) that can activate the NLRC4 inflammasome, process caspase-1 and lead to secretion of mature IL-1beta. This is dependent on the presence of intracellular flagellin. Previous reports have suggested that this activation is independent of extracellular K(+) and not accompanied by leakage of K(+) from the cell, in contrast to activation of the NLRP3 inflammasome. However, non-flagellated strains of Pseudomonas aeruginosa are able to activate NLRC4, suggesting that formation of a pore in the cell membrane by the TTSS apparatus may be sufficient for inflammasome activation. Thus, we set out to determine if extracellular K(+) influenced P. aeruginosa inflammasome activation. We found that raising extracellular K(+) prevented TTSS NLRC4 activation by the non-flagellated P. aeruginosa strain PA103DeltaUDeltaT at concentrations above 90 mm, higher than those reported to inhibit NLRP3 activation. Infection was accompanied by efflux of K(+) from a minority of cells as determined using the K(+)-sensitive fluorophore PBFI, but no formation of a leaky pore. We obtained exactly the same results following infection with Salmonella typhimurium, previously described as independent of extracellular K(+). The inhibitory effect of raised extracellular K(+) on NLRC4 activation thus reflects a requirement for a decrease in intracellular K(+) for this inflammasome component as well as that described for NLRP3. |
| Databáze: | OpenAIRE |
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