Evidence map›Paper›PMID 28832994›Full record

Trial reportClinical and experimental immunology2017

C4B gene influences intestinal microbiota through complement activation in patients with paediatric-onset inflammatory bowel disease.

E Nissilä, K Korpela, A I Lokki, R Paakkanen, S Jokiranta, W M de Vos, M-L Lokki, K-L Kolho, S Meri

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in Clinical and experimental immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 26% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. The complement system in intestinal inflammation and cancer.The Journal of clinical investigation · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. The Impact of Pentraxin 3 on Crohn's Disease Phenotype.International journal of molecular sciences · 2024
    Article
  11. Review
  12. Review
  13. Etiology of IBD-Is It Still a Mystery?International journal of molecular sciences · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. A Protective and Pathogenic Role for Complement During AcuteFrontiers in cellular and infection microbiology · 2021
    Review
  20. 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

9 authors at 1 institution in 1 country.

E NissiläImmunobiology, Research Programs Unit, University of Helsinki, Helsinki, Finland.ORCID 0000-0002-8089-1266
K KorpelaImmunobiology, Research Programs Unit, University of Helsinki, Helsinki, Finland.
A I LokkiImmunobiology, Research Programs Unit, University of Helsinki, Helsinki, Finland.
R PaakkanenTransplantation Laboratory, Medicum, University of Helsinki, Helsinki, Finland.
S JokirantaImmunobiology, Research Programs Unit, University of Helsinki, Helsinki, Finland.
W M de VosImmunobiology, Research Programs Unit, University of Helsinki, Helsinki, Finland.
M-L LokkiTransplantation Laboratory, Medicum, University of Helsinki, Helsinki, Finland.
K-L KolhoChildren's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
S MeriImmunobiology, Research Programs Unit, University of Helsinki, Helsinki, Finland.
University of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement C4 genes are linked to paediatric inflammatory bowel disease (PIBD), but the mechanisms have remained unclear. We examined the influence of C4B gene number on intestinal microbiota and in-vitro serum complement activation by intestinal microbes in PIBD patients. Complement C4A and C4B gene numbers were determined by genomic reverse transcription-polymerase chain reaction (RT-PCR) from 64 patients with PIBD (Crohn's disease or ulcerative colitis). The severity of the disease course was determined from faecal calprotectin levels. Intestinal microbiota was assessed using the HITChip microarray. Complement reactivity in patients was analysed by incubating their sera with Yersinia pseudotuberculosis and Akkermansia muciniphila and determining the levels of C3a and soluble terminal complement complex (SC5b-9) using enzyme immunoassays. The microbiota diversity was wider in patients with no C4B genes than in those with one or two C4B genes, irrespective of intestinal inflammation. C4B and total C4 gene numbers correlated positively with soluble terminal complement complex (TCC, SC5b-9) levels when patient serum samples were stimulated with bacteria. Our results suggest that the C4B gene number associates positively with inflammation in patients with PIBD. Multiple copies of the C4B gene may thus aggravate the IBD-associated dysbiosis through escalated complement reactivity towards the microbiota.

Indexed as

Colitis, UlcerativeComplement ActivationComplement C4bCrohn DiseaseAdolescentChildChild, PreschoolComplement Membrane Attack ComplexFemaleGastrointestinal MicrobiomeGene DosageHumansMaleYersinia pseudotuberculosisComplement C4bComplement Membrane Attack ComplexSC5b-9 protein complexC4 gene numbercomplement activationmicrobiotapaediatric IBD

Identifiers

PMID28832994
PMCPMC5680072
OpenAlexW2745650497

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.