ArticleClinical and experimental immunology2003
Endogenous glucocorticoids attenuate Shiga toxin-2-induced toxicity in a mouse model of haemolytic uraemic syndrome.
Article in Clinical and experimental immunology, 2003. 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, 21 citations in OpenAlex.
- Evolutionary Significance of the Neuroendocrine Stress Axis on Vertebrate Immunity and the Influence of the Microbiome on Early-Life Stress Regulation and Health Outcomes.Frontiers in microbiology · 2021Review
- Therapeutic Strategies to Protect the Central Nervous System against Shiga Toxin from EnterohemorrhagicCurrent neuropharmacology · 2021Article
- Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS).Pediatric nephrology (Berlin, Germany) · 2018Review
- Role of transcriptional coregulator GRIP1 in the anti-inflammatory actions of glucocorticoids.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Lipopolysaccharide renders transgenic mice expressing human serum amyloid P component sensitive to Shiga toxin 2.PloS one · 2011Article
- Review
- Bacillus anthracis lethal toxin represses MMTV promoter activity through transcription factors.Journal of molecular biology · 2009Article
- Pathogenesis of renal disease due to enterohemorrhagic Escherichia coli in germ-free mice.Infection and immunity · 2008Article
- Neural regulation of innate immunity: a coordinated nonspecific host response to pathogens.Nature reviews. Immunology · 2006Review
- Endogenous glucocorticoids modulate neutrophil function in a murine model of haemolytic uraemic syndrome.Clinical and experimental immunology · 2005Article
- Antibody therapy in the management of shiga toxin-induced hemolytic uremic syndrome.Clinical microbiology reviews · 2004Review
- Anthrax lethal factor represses glucocorticoid and progesterone receptor activity.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Neural immune pathways and their connection to inflammatory diseases.Arthritis research & therapy · 2003Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The concept that during an immune challenge the release of glucocorticoids (GC) provides feedback inhibition on evolving immune responses has been drawn primarily from studies of autoimmune and/or inflammatory processes in animal models. The epidemic form of haemolytic uraemic syndrome (HUS) occurs secondary to infection with Gram-negative bacteria that produce Shiga toxin (Stx). Although Stx binding to the specific receptors present on renal tissue is the primary pathogenic mechanism, inflammatory or immune interactions are necessary for the development of the complete form of HUS. The aim of this study was to investigate the influence of endogenous GC on Stx-toxicity in a mouse model. Stx2 was injected into GC-deprived mice and survival rate, renal damage and serum urea levels were evaluated. Plasma corticosterone and cytosolic GC receptor (GR) concentration were also determined at multiple intervals post-Stx2 treatment. Higher sensitivity to Stx2 was observed in mice lacking endogenous GC, evidenced by an increase in mortality rates, circulating urea levels and renal histological damage. Moreover, Stx2 injection was associated with a transient but significant rise in corticosterone secretion. Interestingly, 24 h after Stx inoculation significant increases in total GR were detected in circulating neutrophils. These results indicate that interactions between the neuroendocrine and immune systems can modulate the level of damage significantly during a bacterial infection.
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.