ArticlePloS one2010
Delayed resolution of acute inflammation in ulcerative colitis is associated with elevated cytokine release downstream of TLR4.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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.
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.
Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Ulcerative colitis: the healing power of macrophages.Tissue barriers · 2025Review
- Pouchitis: insight into the pathogenesis and clinical aspects.American journal of translational research · 2022Review
- The Role of Tissue-Resident Macrophages in the Development and Treatment of Inflammatory Bowel Disease.Frontiers in cell and developmental biology · 2022Review
- Anti-inflammation Effects of Sinomenine on Macrophages through Suppressing Activated TLR4/NF-κB Signaling Pathway.Current medical science · 2020Article
- Ornithine Decarboxylase in Macrophages Exacerbates Colitis and Promotes Colitis-Associated Colon Carcinogenesis by Impairing M1 Immune Responses.Cancer research · 2018Article
- Optineurin deficiency in mice contributes to impaired cytokine secretion and neutrophil recruitment in bacteria-driven colitis.Disease models & mechanisms · 2015Article
- Diversity of Intestinal Macrophages in Inflammatory Bowel Diseases.Frontiers in immunology · 2015Review
- ATG4B/autophagin-1 regulates intestinal homeostasis and protects mice from experimental colitis.Autophagy · 2013Article
- Balance of CD8+ CD28+ / CD8+ CD28- T lymphocytes is vital for patients with ulcerative colitis.Digestive diseases and sciences · 2013Article
- A TLR4-interacting peptide inhibits lipopolysaccharide-stimulated inflammatory responses, migration and invasion of colon cancer SW480 cells.Oncoimmunology · 2012Article
- Cytokines, inflammation and colon cancer.Current cancer drug targets · 2011Review
- Rebamipide suppresses TLR-TBK1 signaling pathway resulting in regulating IRF3/7 and IFN-α/β reduction.Journal of clinical biochemistry and nutrition · 2011Article
- Differential expression of TLR2, TLR4 and JNK in mucosa of ileal pouches for ulcerative colitis. Is there a role for bacterial antigen pathway in asymptomatic patients?International journal of clinical and experimental medicine · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundUlcerative colitis (UC) is widely viewed as a leukocyte-mediated disorder. Although strong evidence implicates an exuberant response to microbial components in its pathogenesis, no intrinsic immune defect has been identified and the underlying pathogenic mechanisms remain obscure. METHODOLOGY/PRINCIPAL
findingsThe acute immune response to bacterial injection was determined in UC patients with quiescent disease and directly compared to healthy control subjects. Monocyte-derived macrophages were used to investigate bacterial recognition mechanisms in vitro. An exuberant and protracted acute inflammatory response to bacteria was evident in patients with UC, which coincides with increased systemic levels of CXCL10. Macrophages stimulated with bacteria and Toll-like receptor (TLR) ligands revealed a specific defect in the TLR4 response in UC. The defect resulted in the over-expression of a number of pro-inflammatory molecules under transcriptional control of the adaptor TIR-domain containing adaptor inducing interferon-beta (TRIF).
conclusionThese findings highlight a dysregulated innate immune response with over-expression of molecules associated with leukocyte recruitment and activation that may eventuate in the hallmark chronic immune-mediated inflammation of UC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.