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

ABSTRACT:

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. Nei

SUBMITTER: Ding C 

PROVIDER: S-EPMC6419653 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature