ArticleIntensive care medicine experimental2019
Bradykinin receptor deficiency or antagonism do not impact the host response during gram-negative pneumonia-derived sepsis.
Article in Intensive care medicine experimental, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Capturing resilience from phenotypic deviations: a case study using feed consumption and whole genome data in pigs.BMC genomics · 2024Article
- Pathophysiological dynamics in the contact, coagulation, and complement systems during sepsis: Potential targets for nafamostat mesilate.Journal of intensive medicine · 2024Review
- The Long Pentraxin PTX3 ControlsFrontiers in immunology · 2021Article
- Kinins and Their Receptors in Infectious Diseases.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Prekallikrein inhibits innate immune signaling in the lung and impairs host defense during pneumosepsis in mice.The Journal of pathology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKinins 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.
resultsTo 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.
conclusionsThese data argue against an important role for kinins in the host response to pneumonia-derived sepsis caused by a clinically relevant pathogen.
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