ArticlePediatric nephrology (Berlin, Germany)2012
Toll-like receptor 4 expression on circulating leucocytes in hemolytic uremic syndrome.
Article in Pediatric nephrology (Berlin, Germany), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 17 citations in OpenAlex.
- TLR4: A Potential Therapeutic Target in the Experimental Pathogenesis of Hemolytic-Uremic Syndrome.International journal of molecular sciences · 2026Article
- Toll-like Receptor 4 in Acute Kidney Injury.International journal of molecular sciences · 2023Review
- Severely ill pediatric patients with Shiga toxin-associated hemolytic uremic syndrome (STEC-HUS) who suffered from multiple organ involvement in the early stage.Pediatric nephrology (Berlin, Germany) · 2021Article
- Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS).Pediatric nephrology (Berlin, Germany) · 2018Review
- Basic inflammatory indices and chosen neutrophil receptors expression in chronic haemodialysed patients.Central-European journal of immunology · 2018Article
- Mediators and mechanisms of heat shock protein 70 based cytoprotection in obstructive nephropathy.Cell stress & chaperones · 2015Review
- Prophylactic vaccinations in chronic kidney disease: Current status.Human vaccines & immunotherapeutics · 2015Review
- Natural killer T (NKT) cells accelerate Shiga toxin type 2 (Stx2) pathology in mice.Frontiers in microbiology · 2015Article
- Acute kidney injury: what part do toll-like receptors play?International journal of nephrology and renovascular disease · 2014Review
- Hemolytic uremic syndrome: toxins, vessels, and inflammation.Frontiers in medicine · 2014Review
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
No grant is acknowledged in the PubMed record.
Abstract
Lipopolysaccharide stimulation of toll-like receptor 4 (TLR4) activates signal transduction pathways leading to proinflammatory cytokine secretion. We investigated TLR4 surface receptor expression on peripheral blood neutrophils and monocytes and their ability to modulate inflammatory cytokine release in 15 patients 1, 3, and 10 days after hemolytic uremic syndrome (HUS) onset. Seven patients with Escherichia coli (EHEC)-associated diarrhea and seven healthy controls were also studied. Isolated leucocytes from HUS-onset patients exhibited significantly higher messenger RNA (mRNA) TLR4 expression than controls. Moreover, TLR4 protein expression on neutrophils, determined by flow cytometry, was upregulated, driving dependent proinflammatory cytokine, tumor necrosis factor alpha (TNF-α), and interleukin 8 (IL-8) increase, and decreased anti-inflammatory IL-10 release at HUS onset compared with patients with EHEC diarrhea and controls. TLR4 expression on neutrophils was positively correlated with serum TNF-α levels. Conversely, significant reduction of neutrophil TLR4 receptor expression and lack of cytokine-responsive element activation was shown in patients 3 and 10 days after HUS onset. No differences were demonstrated in TLR4 receptor expression on monocytes among the studied groups. Our results suggest TLR4 expression may be differently regulated on neutrophils and monocytes. They could be dynamically modulated across the early development of HUS on neutrophils, resulting in negative regulation preceded by TLR4 overactivation.
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.