Original Investigation

Medical Microbiology and Immunology

, Volume 197, Issue 1, pp 39-44

First online:

Induction of experimental cerebral malaria is independent of TLR2/4/9

  • Bernd LepeniesAffiliated withDepartment of Immunology, Bernhard Nocht Institute for Tropical Medicine
  • , Jakob P. CramerAffiliated withDepartment of Medicine, University Medical Center Hamburg-Eppendorf, IBernhard-Nocht-Institute for Tropical Medicine, Clinical Research Group
  • , Gerd D. BurchardAffiliated withDepartment of Medicine, University Medical Center Hamburg-Eppendorf, IBernhard-Nocht-Institute for Tropical Medicine, Clinical Research Group
  • , Hermann WagnerAffiliated withInstitute of Medical Microbiology, Immunology and Hygiene, Technical University of Munich
  • , Carsten J. KirschningAffiliated withInstitute of Medical Microbiology, Immunology and Hygiene, Technical University of Munich
  • , Thomas JacobsAffiliated withDepartment of Immunology, Bernhard Nocht Institute for Tropical Medicine Email author 

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Abstract

The contribution of the Toll-like receptor (TLR) cascade to the pathogenesis of cerebral malaria (CM) is controversially discussed. TLR2 and TLR9 were reported to be involved in the induction of CM in a study while recently TLR signaling was shown to be dispensable for the development of CM. Using Plasmodium berghei ANKA (PbA) infection of mice as a model of CM, we demonstrate here that the induction of CM is independent of TLR2, 4 and 9. Using triple TLR2/4/9-deficient mice, we exclude synergistic effects between the single TLRs that have been previously implicated with malaria pathology. In conclusion, this study shows that the activation of the innate immune response and the development of CM is not dependent on the engagement of TLR2/4/9.

Keywords

Cerebral malaria TLR Innate immunity Inflammation Transgenic/knockout mice