Evidence map›Paper›PMID 9918337›Full record

ArticleCanadian journal of veterinary research = Revue canadienne de recherche veterinaire1999

Pathogenesis of porcine Actinobacillus pleuropneumonia, part II: roles of proinflammatory cytokines.

H Huang, A A Potter, M Campos, F A Leighton, P J Willson, D M Haines, W D Yates

Open access · greenAbstract read
In one paragraph

Article in Canadian journal of veterinary research = Revue canadienne de recherche veterinaire, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Journal of veterinary science · 2018
    Article
  6. Article
  7. Article
  8. Article
  9. Acute-phase proteins: As diagnostic tool.Journal of pharmacy & bioallied sciences · 2011
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Immunology of the porcine respiratory disease complex.The Veterinary clinics of North America. Food animal practice · 2001
    Review
  16. Article
  17. Article
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

7 authors at 1 institution in 1 country.

H HuangDepartment of Veterinary Pathology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon. huangho@em.agr.ca
A A Potter
M Campos
F A Leighton
P J Willson
D M Haines
W D Yates
University of Saskatchewan · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The in vitro production of proinflammatory cytokines after stimulation with Actinobacillus pleuropneumoniae and the relation of these cytokines in vivo with the disease caused by A. pleuropneumoniae were investigated. Within 24 h, in vitro stimulation by A. pleuropneumoniae (serotype 1) preparations, including killed bacteria, bacterial culture supernatant, lipopolysaccharide, and bacterial extracts, porcine pulmonary alveolar macrophages (PAM) produced significant (P < 0.05) amounts of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) as measured by bioassays. The supernatants containing interleukin-8 from PAM after stimulation by bacterial preparations showed significant neutrophil chemotaxis, while bacterial preparations alone did not. After in vivo infection with A. pleuropneumoniae, the mean levels of TNF-alpha and IL-1 in serum, as measured by bioassays, were elevated 37- to 27836-fold for TNF-alpha and 11- to 5941-fold higher for IL-1 within 4 d post-infection, depending on the treatments, and remained elevated up to Day 7. Both cytokines were also detected in porcine lungs by bioassays and immunocytochemistry. The results indicated that both secreted and surface components of A. pleuropneumoniae can stimulate PAM to produce proinflammatory mediators. Neutrophil chemoattractants rather than bacterial components are the major factor causing acute lung inflammation. The elevation of TNF-alpha and IL-1 in pigs occurred coincident with the onset of acute clinical disease.

Indexed as

Actinobacillus InfectionsActinobacillus pleuropneumoniaeAnimalsChemotactic FactorsImmunohistochemistryInflammationInterleukin-1LungMacrophages, AlveolarSwineSwine DiseasesTumor Necrosis Factor-alphaChemotactic FactorsInterleukin-1Tumor Necrosis Factor-alpha

Identifiers

PMID9918337
PMCPMC1189518
OpenAlexW1547043798

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.