ArticleBritish journal of pharmacology2013
Exacerbation of DSS-induced colitis in mice lacking kinin B(1) receptors through compensatory up-regulation of kinin B(2) receptors: the role of tight junctions and intestinal homeostasis.
Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Gut microbiota metabolite butyric acid alleviatedBurns & trauma · 2026Article
- KLK1 as an Epithelial-Specific Brake Inhibits Colorectal Tumorigenesis by Suppressing B1R-Mediated Fibroblast Phenotypic Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Dextran sodium sulfate-induced colitis in male BALB/c mice leads to albuminuria and increased markers of inflammation and tissue damage in the kidney.Physiological reports · 2025Article
- The pathogens of secondary infection in septic patients share a similar genotype to those that predominate in the gut.Critical care (London, England) · 2022Observational
- Kinin B1 receptor deficiency protects mice fed by cafeteria diet from abnormal glucose homeostasis.PloS one · 2022Article
- Bradykinin receptor deficiency or antagonism do not impact the host response during gram-negative pneumonia-derived sepsis.Intensive care medicine experimental · 2019Article
- Activation of the Kinin B1 Receptor by Its Agonist Reduces Melanoma Metastasis by Playing a Dual Effect on Tumor Cells and Host Immune Response.Frontiers in pharmacology · 2019Article
- Androgen and Androgen Receptor as Enhancers of M2 Macrophage Polarization in Allergic Lung Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Blockade of Bradykinin receptors worsens the dystrophic phenotype of mdx mice: differential effects for B1 and B2 receptors.Journal of cell communication and signaling · 2018Article
- The Biased G-Protein-Coupled Receptor Agonism Bridges the Gap between the Insulin Receptor and the Metabolic Syndrome.International journal of molecular sciences · 2018Review
- Relationship between G proteins coupled receptors and tight junctions.Tissue barriers · 2018Review
- The Gut-Kidney Axis: Putative Interconnections Between Gastrointestinal and Renal Disorders.Frontiers in endocrinology · 2018Review
- Primary Role for Kinin BMolecular neurobiology · 2017Article
- Genistein improves inflammatory response and colonic function through NF-κB signal in DSS-induced colonic injury.Oncotarget · 2017Article
- Neuroprotective effect of kinin B1 receptor activation in acute cerebral ischemia in diabetic mice.Scientific reports · 2017Article
- Signaling pathways induced by serine proteases to increase intestinal epithelial barrier function.PloS one · 2017Article
- Lack of kinin B₁ receptor potentiates leptin action in the liver.Journal of molecular medicine (Berlin, Germany) · 2013Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeKinins are pro-inflammatory peptides that are released during tissue injury, including that caused by inflammatory bowel disease. Herein, we assessed the role and underlying mechanisms through which the absence of kinin B(1) receptors exacerbates the development of dextran sulfate sodium (DSS)-induced colitis in mice. EXPERIMENTAL APPROACH: B(1) and B(2) receptor antagonists and B(1) receptor knockout mice (B1(-/-) ) were used to assess the involvement of B(1) and B(2) receptor signalling in a DSS-colitis. B(1) receptor, B(2) receptor, occludin and claudin-4 expression, cytokine levels and cell permeability were evaluated in colon from wild-type (WT) and B1(-/-) mice. KEY
resultsDSS-induced colitis was significantly exacerbated in B1(-/-) compared with WT mice. IL-1β, IFN-γ, keratinocyte-derived chemokine and macrophage inflammatory protein-2 were markedly increased in the colon from DSS-treated B1(-/-) compared with DSS-treated WT mice. Treatment of WT mice with a selective B(1) receptor antagonist, DALBK or SSR240612, had no effect on DSS-induced colitis. Of note, B(2) receptor mRNA expression was significantly up-regulated in colonic tissue from the B1(-/-) mice after DSS administration. Moreover, treatment with a selective B(2) receptor antagonist prevented the exacerbation of colitis in B1(-/-) mice following DSS administration. The water- or DSS-treated B1(-/-) mice showed a decrease in occludin gene expression, which was partially prevented by the B(2) receptor antagonist. CONCLUSIONS AND IMPLICATIONS: A loss of B(1) receptors markedly exacerbates the severity of DSS-induced colitis in mice. The increased susceptibility of B1(-/-) may be associated with compensatory overexpression of B(2) receptors, which, in turn, modulates tight junction expression.
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