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Record W4396991506 · doi:10.1681/asn.20223311s1518b

Lack of Complement Factor H Contributes to Endothelial Cell Injury in Shiga Toxin Haemolytic Uraemic Syndrome

2022· article· en· W4396991506 on OpenAlexaff
Emily E. Bowen, Jenny Hurcombe, Fern Barrington, Louise K. Farmer, Carolina G. Ortiz-Sandoval, Valentina Bruno, Niyousha Rostam Shirazi, Gavin I. Welsh, Christoph Licht, Moin A. Saleem, Richard J. Coward

Bibliographic record

VenueJournal of the American Society of Nephrology · 2022
Typearticle
Languageen
FieldImmunology and Microbiology
TopicComplement system in diseases
Canadian institutionsSickKids Foundation
Fundersnot available
KeywordsHaemolytic-uraemic syndromeShiga toxinComplement systemImmunologyToxinComplement (music)MedicineAtypical hemolytic uremic syndromeMicrobiologyBiologyAntibodyBiochemistryEscherichia coli

Abstract

fetched live from OpenAlex

Background: Haemolytic uraemic syndrome (HUS) is a thrombotic microangiopathy that has a predilection for the kidney. In 90% of cases, HUS follows gastroenteritis secondary to infection with Shiga toxin (Stx) producing bacteria such as Escherichia coli. STEC HUS is the leading cause of acute kidney injury in children with a mortality of 5%. We have previously shown endothelial cell complement activation in a PodGb3 mouse model of STEC HUS. Here we build upon these findings to show that a reduction in glomerular endothelial CFH occurs both in our animal model and in-vitro co-culture models. Methods: To demonstrate that the podocyte Stx receptor (Gb3) is sufficient to trigger the development of HUS, we used conditional gene targeting to engineer human Gb3 expression specifically in the podocytes of mice (PodGb3). Using an in-vitro human glomerular cell co-culture model we evaluated the effects of Stx on endothelial cell injury, complement activation (C3b, C5b-9) and regulation (CD46, CD55, CFH). Results: Following intraperitoneal Stx, PodGb3 mice recapitulate all of the histopathological features of HUS. Further interrogation demonstrated glomerular endothelial cell complement activation, loss of CFH protection and rescue of the HUS phenotype following C5 inhibitor treatment. Interestingly, in co-culture studies Stx caused a reduction in glomerular endothelial CFH that was only seen in the presence of co-culture with podocytes. Conclusions: These observations provide compelling evidence for the importance of podocyte-glomerular endothelial cell cross-talk in the development of STEC HUS and suggest a possible therapeutic role for complement inhibition in patients with this devastating disease. Funding: Other NIH Support - Kidney Research UK, Academy of Medical Sciences, BMSA foundation Grant Lack of Complement Factor H contributes to endothelial cell injury in Shiga toxin Haemolytic Uraemic Syndrome (HUS): supporting Figure 1.Figure 1:: PodGB3 mice given intraperitoneal Shiga toxin show evidence of endothelial complement activation (C3b) and loss of CFH protection.Day 10 post-IP Stx glomerular immunofluorescence analysis for C3b and complemtn factor H (green) with co-staining for nephrin (red) in PodGb3 mice and controls. Scale bar, 25 μm.Fold change in corrected total glomerular fluorescence intensity (CTGF) was calculated using Image J analysis for C3b and complement factor H deposition in the glomerulus. PodGb3 n=3, controls n=3 with 30 glomeruli per mouse analysed. Unpaired T-test p value ***<0.0001.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.001
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: none
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.798
Threshold uncertainty score0.741

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0010.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0010.001
Bibliometrics0.0000.000
Science and technology studies0.0000.001
Scholarly communication0.0000.000
Open science0.0010.001
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0010.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.028
GPT teacher head0.293
Teacher spread0.265 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one teacher head, not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2022
Admission routes1
Has abstractyes

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