Journal article
Cutting Edge: Inhibition of IL-6 Trans-Signaling Protects from Malaria-Induced Lethality in Mice
The Journal of immunology (1950), Vol.188(9), pp.4141-4144
05/01/2012
DOI: 10.4049/jimmunol.1102137
PMID: 22467660
Abstract
Circulating IL-6 levels correlate with the severity of blood-stage malaria in humans and mouse models, but the impact of IL-6 classic signaling through membrane IL-6R alpha, as well as IL-6 trans-signaling through soluble IL-6R alpha, on the outcome of malaria has remained unknown. In this study, we created IL-6R alpha-deficient mice that exhibit a 50% survival of otherwise lethal blood-stage malaria of the genus Plasmodium chabaudi. Inducing IL-6 trans-signaling by injection of mouse recombinant soluble IL-6R alpha in IL-6R alpha-deficient mice restores the lethal outcome to malaria infection. In contrast, inhibition of IL-6 trans-signaling via injection of recombinant sGP130Fc protein in control mice results in a 40% survival rate. Our data demonstrate that IL-6 trans-signaling, rather than classic IL-6 signaling, contributes to malaria-induced lethality in mice, preceded by an increased inflammatory response. Therefore, inhibition of IL-6 trans-signaling may serve as a novel promising therapeutic basis to combat malaria. The Journal of Immunology, 2012, 188: 4141-4144.
Details
- Title: Subtitle
- Cutting Edge: Inhibition of IL-6 Trans-Signaling Protects from Malaria-Induced Lethality in Mice
- Creators
- Claudia M. Wunderlich - Max Planck SocietyDenis Delic - Heinrich Heine University DüsseldorfKristina Behnke - Heinrich Heine University DüsseldorfAndreas Meryk - Heinrich Heine University DüsseldorfPeter Stroehle - Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated DiseasesBhagirath Chaurasia - Max Planck SocietySaleh Al-Quraishy - King Saud UniversityFrank Wunderlich - Heinrich Heine University DüsseldorfJens C. Bruening - Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated DiseasesF. Thomas Wunderlich - Max Planck Society
- Resource Type
- Journal article
- Publication Details
- The Journal of immunology (1950), Vol.188(9), pp.4141-4144
- DOI
- 10.4049/jimmunol.1102137
- PMID
- 22467660
- NLM abbreviation
- J Immunol
- ISSN
- 0022-1767
- eISSN
- 1550-6606
- Publisher
- Amer Assoc Immunologists
- Number of pages
- 4
- Grant note
- FP7-HEALTH-2009-241592 / European Union; European Commission BR 1492/7-1; SFB 832 A15; GRK 1427 / Deutsche Forschungsgemeinschaft (DFG); German Research Foundation (DFG) Competence Network for Adipositas (Neuro-target) D1; B2 / Center for Molecular Medicine and Cluster of Excellence Cellular Stress Responses in Aging-Associated Diseases, University of Cologne FKZ01GIO845 / Federal Ministry of Education and Research; Federal Ministry of Education & Research (BMBF)
- Language
- English
- Date published
- 05/01/2012
- Academic Unit
- Fraternal Order of Eagles Diabetes Research Center; Endocrinology and Metabolism; Internal Medicine
- Record Identifier
- 9984359674202771
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