Evidence map›Paper›PMID 28694696›Full record

ReviewInternational journal of chronic obstructive pulmonary disease2017

Th17 profile in COPD exacerbations.

Marco Antonio Ponce-Gallegos, Alejandra Ramírez-Venegas, Ramcés Falfán-Valencia

Open access · goldAbstract readReview
In one paragraph

Review in International journal of chronic obstructive pulmonary disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Frontiers in immunology · 2024
    Review
  11. Review
  12. Article
  13. Article
  14. Observational
  15. Article
  16. Research on the Association Between Periodontitis and COPD.International journal of chronic obstructive pulmonary disease · 2023
    Review
  17. The role of Th17 cells: explanation of relationship between periodontitis and COPD?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
  18. Article
  19. Review
  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

3 authors at 2 institutions in 2 countries.

Marco Antonio Ponce-GallegosHLA Laboratory, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City, Mexico.
Alejandra Ramírez-VenegasTobacco Smoking and COPD Research Department, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City, Mexico.
Ramcés Falfán-ValenciaHLA Laboratory, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City, Mexico.
Instituto Nacional de Enfermedades Respiratorias · MXUniversidad Autónoma de Nayarit · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COPD is characterized by an ongoing inflammatory process of the airways that leads to obstruction or limitation of airflow. It is mainly associated with exposure to cigarette smoke. In addition, it is considered, at present, a serious public health problem, ranking fourth in mortality worldwide. Many cells participate in the pathophysiology of COPD, the most important are neutrophils, macrophages and CD4+ and CD8+ T cells. Neutrophil migration to the inflammation area could be mediated largely by cytokines related to CD4+ Th17 lymphocytes, because it has been shown that IL-17A, IL-17F and IL-22 act as inducers for CXCL8, CXCL1, CXCL5, G-CSF, and GM-CSF secretion by epithelial cells of the airways. The aims of these molecules are differentiation, proliferation and recruitment of neutrophils. Furthermore, it is believed that CD4+ lymphocytes Th17 may be involved in protection against pathogens for which Th1 and Th2 are not prepared to fight. In COPD exacerbations, there is an increased cellularity in the lung region and respiratory tract. Therefore, the increase in the number of neutrophils and macrophages in the airways and the increase in proinflammatory cytokines are directly related to the severity of exacerbations and that is the importance of the functions of Th17 profile in this entity.

Indexed as

Lymphocyte ActivationAdaptive ImmunityAnimalsBacterial InfectionsChemotaxisCigarette SmokingCytokinesEpithelial CellsHumansImmunity, InnateLungMacrophagesNeutrophil InfiltrationNeutrophilsPhenotypePulmonary Disease, Chronic ObstructiveCytokinesbacteriaIL-17AIL-17FIL-22tobacco smokingvirus

Identifiers

PMID28694696
PMCPMC5491572
OpenAlexW2643696376

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.