Evidence map›Paper›PMID 24585052›Full record

ReviewJournal of microbiology (Seoul, Korea)2014

Chronic obstructive pulmonary disease (COPD): evaluation from clinical, immunological and bacterial pathogenesis perspectives.

Daniel J Hassett, Michael T Borchers, Ralph J Panos

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of microbiology (Seoul, Korea), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
7.2field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 79 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Microbiology spectrum · 2024
    Article
  8. Frontiers in immunology · 2024
    Review
  9. Review
  10. bioRxiv : the preprint server for biology · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. The Building Blocks of Antimicrobial Resistance inFrontiers in cellular and infection microbiology · 2021
    Review
  17. Biofilm dispersion.Nature reviews. Microbiology · 2020
    Review
  18. Clinical Significance of Carbapenem-TolerantAntibiotics (Basel, Switzerland) · 2020
    Article
  19. Article
  20. ERJ open research · 2020
    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

3 authors at 2 institutions in 1 country.

Daniel J HassettDepartments of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA, Daniel.Hassett@UC.Edu.
Michael T Borchers
Ralph J Panos
Cincinnati VA Medical Center · USUniversity of Cincinnati Medical Center · US

Funding

Shared Mechanisms of Pulmonary Lymphocyte Activation by Bacteria and ToxicantsR01ES015036 · NIEHS · UNIVERSITY OF CINCINNATI · PI BORCHERS, MICHAEL · 2006 to 2010
$2.1M
Novel Reagents in Mouse Models of Autoimmune COPDR21HL109635 · NHLBI · UNIVERSITY OF CINCINNATI · PI BORCHERS, MICHAEL · 2011 to 2012
$432k
BLRD VA I01 BX002347NHLBI NIH HHS R21 HL109635NIEHS NIH HHS R01 ES015036
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD), a disease manifested by significantly impaired airflow, afflicts ∼14.2 million cases in the United States alone with an estimated 63 million people world-wide. Although there are a number of causes, the predominant cause is excessive tobacco smoke. In fact, in China, there have been estimates of 315,000,000 people that smoke. Other less frequent causes are associated with indirect cigarette smoke, air pollutants, biomass fuels, and genetic mutations. COPD is often associated with heart disease, lung cancer, osteoporosis and conditions can worsen in patients with sudden falls. COPD also affects both innate and adaptive immune processes. Cigarette smoke increases the expression of matrix metalloproteases and proinflammatory chemokines and increases lung titers of natural killer cells and neutrophils. Yet, neutrophil reactive oxygen species (ROS) mediated by the phagocytic respiratory burst and phagocytosis is impaired by nicotine. In contrast to innate immunity in COPD, dendritic cells represent leukocytes recruited to the lung that link the innate immune responses to adaptive immune responses by activating naïve T cells through antigen presentation. The autoimmune process that is also a significant part of inflammation associated with COPD. Moreover, coupled with restricted FEV1 values, are the prevalence of patients with single or multiple infections by bacteria, viruses and fungi. Finally, we focus on one of the more problematic infectious agents, the Gram-negative opportunistic pathogenic bacterium, Pseudomonas aeruginosa. Specifically, we delve into the development of highly problematic biofilm infections that are highly refractory to conventional antibiotic therapies in COPD. We offer a non-conventional, biocidal treatment that may be effective for COPD airway infections as well as with combinations of current antibiotic regimens for more effective treatment outcomes and relief for patients with COPD.

Indexed as

Anti-Bacterial AgentsBiofilmsDrug TherapyGlobal HealthHumansPseudomonas aeruginosaPseudomonas InfectionsPulmonary Disease, Chronic ObstructiveAnti-Bacterial Agents

Identifiers

PMID24585052
OpenAlexW1986857099

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.