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Background  Kinins are short peptides with a wide range of proinflammatory properties that are generated from kininogens in the so-called kallikrein-kinin system. Kinins exert their biological activities through stimulation of two distinct receptor subtypes, the kinin or bradykinin B1 and B2 receptors (B1R, B2R). Acute challenge models have implicated B1R and B2R in the pathogenesis of sepsis. However, their role in the host response during sepsis originating from the lung is not known.    Results  To determine the role of B1R and B2R in pneumonia-derived sepsis, B1R/B2R-deficient mice and wild-type mice treated with the B1R antagonist R-715 or the B2R antagonist HOE-140 were studied after infection with the common gram-negative pathogen  Klebsiella pneumoniae  via the airways. Neither B1R/B2R deficiency nor B1R or B2R inhibition influenced bacterial growth at the primary site of infection or dissemination to distant body sites. In addition, B1R/B2R deficiency or inhibition did not impact local or systemic inflammatory responses during  Klebsiella  induced pneumosepsis.    Conclusions  These data argue against an important role for kinins in the host response to pneumonia-derived sepsis caused by a clinically relevant pathogen.    Electronic supplementary material  The online version of this article (10.1186/s40635-019-0228-3) contains supplementary material, which is available to authorized users.

Bradykinin receptor deficiency or antagonism do not impact the host response during gram-negative pneumonia-derived sepsis