Print Email Facebook Twitter The bradykinin B2 receptor in the early immune response against Listeria infection Title The bradykinin B2 receptor in the early immune response against Listeria infection Author TNO Defensie en Veiligheid Kaman, W.E. Wolterink, A.F.W.M. Bader, M. Boele, L.C.L. van der Kleij, D. Publication year 2009 Abstract The endogenous danger signal bradykinin was recently found implicated in the development of immunity against parasites via dendritic cells. We here report an essential role of the B2 (B2R) bradykinin receptor in the early immune response against Listeria infection. Mice deficient in B2R (B2R-/- mice) were shown to suffer from increased hepatic bacterial burden and concomitant dramatic weight loss during infection with Listeria monocytogenes. Levels of cytokines known to play a pivotal role in the early phase immune response against L. monocytogenes, IL-12p70 and IFN-γ, were reduced in B2R-/- mice. To extend these findings to the human system, we show that bradykinin potentiates the production of IL-12p70 in human monocyte-derived dendritic cells. Thus, we show that bradykinin and the B2R play a role in early innate immune functions during bacterial infection. © 2008 Springer-Verlag. Subject BradykininCytokinesKnock out miceListeria monocytogenesBradykinin B2 receptorGamma interferonInterleukin 12p70Animal experimentAnimal modelArticleControlled studyCytokine productionDendritic cellImmune responseLsteria monocytogenesListeriosisMonocyteMouseNonhumanPriority journalProtein functionWeight reductionAnimalsBody WeightBradykininCells, CulturedCytokinesDendritic CellsHumansInterferon-gammaInterleukin-12Listeria InfectionsListeria monocytogenesLiverMiceMice, KnockoutReceptor, Bradykinin B2 To reference this document use: http://resolver.tudelft.nl/uuid:09332dd4-620d-46fb-a233-bf7c60d84992 DOI https://doi.org/10.1007/s00430-008-0103-4 TNO identifier 241382 ISSN 0300-8584 Source Medical Microbiology and Immunology, 198 (198), 39-46 Document type article Files To receive the publication files, please send an e-mail request to TNO Library.