Evidence map›Paper›PMID 9863482›Full record

ArticleGut1998

Kallikrein-kininogen system activation and bradykinin (B2) receptors in indomethacin induced enterocolitis in genetically susceptible Lewis rats.

A Stadnicki, R B Sartor, R Janardham, I Stadnicka, A A Adam, C Blais, R W Colman

Open access · bronzeAbstract read
In one paragraph

Article in Gut, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

A StadnickiSol Sherry Thrombosis Research Center, Temple University School of Medicine, Philadelphia, PA, USA.
R B Sartor
R Janardham
I Stadnicka
A A Adam
C Blais
R W Colman
Temple University · USUniversity of North Carolina at Chapel Hill · USUniversité de Montréal · CA

Funding

PILOT AND FEASIBILITY STUDIESP30DK034987 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ROBERT S. SANDLER · 1985 to 2026
$30.5M
MECHANISMS OF COLITIS INDUCED BY DEFINED BACTERIAL FLORAR01DK040249 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SARTOR, RYAN B · 1989 to 2011
$3.0M
KALLIKREIN/KININ SYSTEM IN INFLAMMATORY BOWEL DISEASER01DK043735 · NIDDK · TEMPLE UNIVERSITY · PI COLMAN, ROBERT W · 1992 to 2001
$420k
NIDDK NIH HHS DK34987NIDDK NIH HHS DK40249NIDDK NIH HHS DK43735
6 · The paper itself

Abstract

backgroundThe plasma kallikrein-kinin (K-K) system is activated in acute and chronic relapsing intestinal inflammation induced in Lewis rats by intramural injection of exogenous bacterial components.

aimsTo determine whether this effect is model specific, K-K system activation was investigated in a modified indomethacin induced enterocolitis model, as well as bradykinin 2 (B2) receptor distribution in the normal and acutely inflamed intestine.

methodsLewis rats injected with daily sublethal doses of indomethacin for two days developed acute (two days) and chronic (14 days) intestinal inflammation. Plasma prekallikrein (amidolytic), high molecular weight kininogen (HK, coagulant) and cleavage of HK (western blot) were assayed to detect K-K activation.

resultsLiver and spleen weights were significantly higher, and body weights and haematocrit values were significantly lower in the indomethacin group than in the control group. During both acute and chronic phases, rats displayed K-K system activation manifested by a significant decrease in plasma prekallikrein and HK functional levels, and by HK cleavage. Plasma T kininogen (a major acute phase protein) was significantly elevated. B2 receptors were identified in both normal and inflammatory intestine with more prominent specific immunohistochemical staining in the acutely inflamed tissue.

conclusionsK-K system activation occurs in association with both acute and chronic phases of intestinal injury, regardless of the triggering agent, suggesting that activation of this system is integrally involved in intestinal inflammation in genetically susceptible hosts. Localisation of B2 receptors across intestinal layers provides a structural basis for the kinin function in the intestine.

Indexed as

Acute DiseaseAnimalsAnti-Inflammatory Agents, Non-SteroidalChronic DiseaseEnterocolitisFemaleGenetic Predisposition to DiseaseImmunohistochemistryIndomethacinIntestine, SmallKallikrein-Kinin SystemKininogen, High-Molecular-WeightKininogensPrekallikreinRatsRats, Inbred LewAnti-Inflammatory Agents, Non-SteroidalIndomethacinKininogen, High-Molecular-WeightKininogensPrekallikreinReceptor, Bradykinin B2Receptors, Bradykinin

Identifiers

PMID9863482
PMCPMC1727239
OpenAlexW2051475922

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.