Evidence map›Paper›PMID 23286938›Full record

ReviewClinical and experimental immunology2013

Immune mechanisms and the impact of the disrupted lung microbiome in chronic bacterial lung infection and bronchiectasis.

R J Boyton, C J Reynolds, K J Quigley, D M Altmann

Open access · greenAbstract readReview
In one paragraph

Review in Clinical and experimental immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. International journal of molecular sciences · 2026
    Review
  3. Review
  4. Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. The Open Challenge ofFrontiers in bioengineering and biotechnology · 2020
    Review
  17. Review
  18. Article
  19. Brazilian consensus on non-cystic fibrosis bronchiectasis.Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia · 2019
    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

4 authors at 2 institutions in 1 country.

R J BoytonLung Immunology Group, Section of Infectious Diseases and Immunity, Hammersmith Campus, Department of Medicine, Centre for Respiratory Infection, Imperial College London, UK. r.boyton@imperial.ac.uk
C J Reynolds
K J Quigley
D M Altmann
Hammersmith Hospital · GBImperial College London · GB

Funding

Biotechnology and Biological Sciences Research Council BB/H005439/1Medical Research Council
6 · The paper itself

Abstract

Recent studies analysing immunogenetics and immune mechanisms controlling susceptibility to chronic bacterial infection in bronchiectasis implicate dysregulated immunity in conjunction with chronic bacterial infection. Bronchiectasis is a structural pathological end-point with many causes and disease associations. In about half of cases it is termed idiopathic, because it is of unknown aetiology. Bronchiectasis is proposed to result from a 'vicious cycle' of chronic bacterial infection and dysregulated inflammation. Paradoxically, both immune deficiency and excess immunity, either in the form of autoimmunity or excessive inflammatory activation, can predispose to disease. It appears to be a part of the spectrum of inflammatory, autoimmune and atopic conditions that have increased in prevalence through the 20th century, attributed variously to the hygiene hypothesis or the 'missing microbiota'. Immunogenetic studies showing a strong association with human leucocyte antigen (HLA)-Cw*03 and HLA-C group 1 homozygosity and combinational analysis of HLA-C and killer immunoglobulin-like receptors (KIR) genes suggests a shift towards activation of natural killer (NK) cells leading to lung damage. The association with HLA-DR1, DQ5 implicates a role for CD4 T cells, possibly operating through influence on susceptibility to specific pathogens. We hypothesize that disruption of the lung microbial ecosystem, by infection, inflammation and/or antibiotic therapy, creates a disturbed, simplified, microbial community ('disrupted microbiota') with downstream consequences for immune function. These events, acting with excessive NK cell activation, create a highly inflammatory lung environment that, in turn, permits the further establishment and maintenance of chronic infection dominated by microbial pathogens. This review discusses the implication of these concepts for the development of therapeutic interventions.

Indexed as

AnimalsBacterial InfectionsBronchiectasisCD4-Positive T-LymphocytesChronic DiseaseGenetic Predisposition to DiseaseHLA-C AntigensHumansKiller Cells, NaturalLungLung DiseasesMetagenomeMicrobial ConsortiaPolymorphism, GeneticReceptors, KIRHLA-C AntigensReceptors, KIR

Identifiers

PMID23286938
PMCPMC3573282
OpenAlexW2123366575

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.