Evidence map›Paper›PMID 23189195›Full record

ArticlePloS one2012

A new role of the complement system: C3 provides protection in a mouse model of lung infection with intracellular Chlamydia psittaci.

Jenny Bode, Pavel Dutow, Kirsten Sommer, Katrin Janik, Silke Glage, Burkhard Tümmler, Antje Munder, Robert Laudeley, Konrad W Sachse, Andreas Klos

Abstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

27 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Complement andFrontiers in immunology · 2021
    Article
  9. Complement andFrontiers in immunology · 2021
    Article
  10. Article
  11. An Ancient Molecular Arms Race:Frontiers in immunology · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

10 authors.

Jenny BodeInstitute of Medical Microbiology and Hospital Epidemiology, Hannover Medical School (MHH), Hannover, Germany.
Pavel Dutow
Kirsten Sommer
Katrin Janik
Silke Glage
Burkhard Tümmler
Antje Munder
Robert Laudeley
Konrad W Sachse
Andreas Klos

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complement system modulates the intensity of innate and specific immunity. While it protects against infections by extracellular bacteria its role in infection with obligate intracellular bacteria, such as the avian and human pathogen Chlamydia (C.) psittaci, is still unknown. In the present study, knockout mice lacking C3 and thus all main complement effector functions were intranasally infected with C. psittaci strain DC15. Clinical parameters, lung histology, and cytokine levels were determined. A subset of infections was additionally performed with mice lacking C5 or C5a receptors. Complement activation occurred before symptoms of pneumonia appeared. Mice lacking C3 were ∼100 times more susceptible to the intracellular bacteria compared to wild-type mice, with all C3(-/-) mice succumbing to infection after day 9. At a low infective dose, C3(-/-) mice became severely ill after an even longer delay, the kinetics suggesting a so far unknown link of complement to the adaptive, protective immune response against chlamydiae. The lethal phenotype of C3(-/-) mice is not based on differences in the anti-chlamydial IgG response (which is slightly delayed) as demonstrated by serum transfer experiments. In addition, during the first week of infection, the absence of C3 was associated with partial protection characterized by reduced weight loss, better clinical score and lower bacterial burden, which might be explained by a different mechanism. Lack of complement functions downstream of C5 had little effect. This study demonstrates for the first time a strong and complex influence of complement effector functions, downstream of C3 and upstream of C5, on the outcome of an infection with intracellular bacteria, such as C. psittaci.

Indexed as

AnimalsBacterial LoadBronchoalveolar Lavage FluidChlamydophila psittaciComplement ActivationComplement C3Complement C5Complement System ProteinsCytokinesDisease SusceptibilityGranulocytesImmunoglobulin GImmunoglobulin MLungMaleMiceComplement C3Complement C5Complement System ProteinsCytokinesImmunoglobulin GImmunoglobulin MPeroxidaseReceptors, Complement

Identifiers

PMID23189195
PMCPMC3506576

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Registered trials

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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.