Evidence map›Paper›PMID 20956586›Full record

ArticleAntimicrobial agents and chemotherapy2011

Anti-Inflammatory benefits of antibiotic-induced neutrophil apoptosis: tulathromycin induces caspase-3-dependent neutrophil programmed cell death and inhibits NF-kappaB signaling and CXCL8 transcription.

Carrie D Fischer, Jennifer K Beatty, Cheryl G Zvaigzne, Douglas W Morck, Merlyn J Lucas, A G Buret

Open access · bronzeAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
  2. Methaphylactic effect of tulathromycin treatment on rumen fluid parameters in feedlot beef cattle.Canadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2016
    Trial
  3. Flavones induce neutrophil apoptosis by down-regulation of Mcl-1 via a proteasomal-dependent pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    Trial
  4. Article
  5. Article
  6. Dalbavancin Boosts the Ability of Neutrophils to Fight Methicillin-ResistantInternational journal of molecular sciences · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Penicillin in oral aphthosis, new insight for an old drug: A randomized, double-blind, controlled clinical trial.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 2 institutions in 2 countries.

Carrie D FischerUniversity of Calgary, Department of Biological Sciences, Calgary, Alberta, Canada.
Jennifer K Beatty
Cheryl G Zvaigzne
Douglas W Morck
Merlyn J Lucas
A G Buret
University of Calgary · CAPfizer (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clearance of apoptotic neutrophils is a central feature of the resolution of inflammation. Findings indicate that immuno-modulation and induction of neutrophil apoptosis by macrolide antibiotics generate anti-inflammatory benefits via mechanisms that remain obscure. Tulathromycin (TUL), a new antimicrobial agent for bovine respiratory disease, offers superior clinical efficacy for reasons not fully understood. The aim of this study was to identify the immuno-modulating effects of tulathromycin and, in this process, to establish tulathromycin as a new model for characterizing the novel anti-inflammatory properties of antibiotics. Bronchoalveolar lavage specimens were collected from Holstein calves 3 and 24 h postinfection, challenged intratracheally with live Mannheimia haemolytica (2 × 10(7) CFU), and treated with vehicle or tulathromycin (2.5 mg/kg body weight). Terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) staining and enzyme-linked immunosorbent assay (ELISA) revealed that tulathromycin treatment significantly increased leukocyte apoptosis and reduced levels of proinflammatory leukotriene B(4) in M. haemolytica-challenged calves. In vitro, tulathromycin concentration dependently induced apoptosis in freshly isolated bovine neutrophils from healthy steers in a capase-3-dependent manner but failed to induce apoptosis in bovine fibroblasts, epithelial cells, and endothelial cells, as well as freshly isolated bovine blood monocytes and monocyte-derived macrophages. The proapoptotic effects of TUL were also, in part, drug specific; equimolar concentrations of penicillin G, oxytetracycline, and ceftiofur failed to cause apoptosis in bovine neutrophils. In addition, tulathromycin significantly reduced levels of phosphorylated IκBα, nuclear translocation of NF-κB p65, and mRNA levels of proinflammatory interleukin-8 in lipopolysaccharide (LPS)-stimulated bovine neutrophils. The findings illustrate novel mechanisms through which tulathromycin confers anti-inflammatory benefits.

Indexed as

AnimalsAnti-Bacterial AgentsAnti-Inflammatory AgentsApoptosisBlotting, WesternCaspase 3CattleCell LineCells, CulturedDisaccharidesDNA FragmentationEnzyme-Linked Immunosorbent AssayHeterocyclic CompoundsIn Situ Nick-End LabelingInterleukin-8Leukotriene B4Anti-Bacterial AgentsAnti-Inflammatory AgentsCaspase 3DisaccharidesHeterocyclic CompoundsInterleukin-8Leukotriene B4MacrolidesNF-kappa Btulathromycin

Identifiers

PMID20956586
PMCPMC3019645
OpenAlexW2117925806

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.