Evidence map›Paper›PMID 26512700›Full record

ArticlePathogens (Basel, Switzerland)2015

Differential Contributions of the Complement Anaphylotoxin Receptors C5aR1 and C5aR2 to the Early Innate Immune Response against Staphylococcus aureus Infection.

Sarah A Horst, Andreas Itzek, Andreas Klos, Andreas Beineke, Eva Medina

Open access · goldAbstract read
In one paragraph

Article in Pathogens (Basel, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Protective role of host complement system inFrontiers in immunology · 2022
    Article
  6. A Narrative Review on the Role ofOpen forum infectious diseases · 2021
    Review
  7. Article
  8. Article
  9. Review
  10. 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

5 authors at 3 institutions in 1 country.

Sarah A HorstInfection Immunology Research Group, Helmholtz Centre for Infection Research, Inhoffenstrasse 7, 38124 Braunschweig, Germany. sarah.horst@gmx.de.
Andreas ItzekMicrobial Interactions and Processes Research Group, Helmholtz Centre for Infection Research, Inhoffenstrasse 7, 38124 Braunschweig, Germany. andreas.itzek@helmholtz-hzi.de.
Andreas KlosInstitute of Medical Microbiology and Hospital Epidemiology, Medical School Hannover, Hannover, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany. Klos.Andreas@mh-hannover.de.
Andreas BeinekeInstitute for Pathology, University of Veterinary Medicine Hannover, Bünteweg 17, 30559 Hannover, Germany. andreas.beineke@tiho-hannover.de.
Eva MedinaInfection Immunology Research Group, Helmholtz Centre for Infection Research, Inhoffenstrasse 7, 38124 Braunschweig, Germany. eva.medina@helmholtz-hzi.de.
Helmholtz Centre for Infection Research · DEMedizinische Hochschule Hannover · DEUniversity of Veterinary Medicine Hannover, Foundation · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complement anaphylatoxin C5a contributes to host defense against Staphylococcus aureus. In this study, we investigated the functional role of the two known C5a receptors, C5aR1 and C5aR2, in the host response to S. aureus. We found that C5aR1(-/)(-) mice exhibited greater susceptibility to S. aureus bloodstream infection than wild type and C5aR2(-/)(-) mice, as demonstrated by the significantly higher bacterial loads in the kidneys and heart at 24 h of infection, and by the higher levels of inflammatory IL-6 in serum. Histological and immunohistochemistry investigation of infected kidneys at 24 h after bacterial inoculation revealed a discrete infiltration of neutrophils in wild type mice but already well-developed abscesses consisting of bacterial clusters surrounded by a large number of neutrophils in both C5aR1(-/)(-) and C5aR2(-/)(-) mice. Furthermore, blood neutrophils from C5aR1(-/)(-) mice were less efficient than those from wild type or C5aR2(-/)(-) mice at killing S. aureus. The requirement of C5aR1 for efficient killing of S. aureus was also demonstrated in human blood after disrupting C5a-C5aR1 signaling using specific inhibitors. These results demonstrated a role for C5aR1 in S. aureus clearance as well as a role for both C5aR1 and C5aR2 in the orchestration of the inflammatory response during infection.

Indexed as

C5aC5aR1C5aR2complement systemneutrophilsStaphylococcus aureus

Identifiers

PMID26512700
PMCPMC4693161
OpenAlexW2177675608

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.