Evidence map›Paper›PMID 32203101›Full record

ReviewExperimental & molecular medicine2020

The impact of bacteria-derived ultrafine dust particles on pulmonary diseases.

Jinho Yang, Eun Kyoung Kim, Hyeon Ju Park, Andrea McDowell, Yoon-Keun Kim

Open access · goldAbstract readReview
In one paragraph

Review in Experimental & molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.7field-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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Infectious Diseases Associated with Desert Dust Outbreaks: A Systematic Review.International journal of environmental research and public health · 2022
    Pooled it
  2. Article
  3. Article
  4. Review
  5. Microbial extracellular vesicles in the lung: friends in health, agents in disease.Extracellular vesicles and circulating nucleic acids · 2026
    Review
  6. Epidemiological Trends and Projections of PMInternational journal of chronic obstructive pulmonary disease · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. The Effects and Pathogenesis of PM2.5 and Its Components on Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023
    Review
  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

5 authors at 2 institutions in 2 countries.

Jinho YangInstitute of MD Healthcare Inc., Seoul, Republic of Korea.ORCID http://orcid.org/0000-0001-7207-6846
Eun Kyoung KimInstitute of MD Healthcare Inc., Seoul, Republic of Korea.
Hyeon Ju ParkInstitute of MD Healthcare Inc., Seoul, Republic of Korea.
Andrea McDowellInstitute of MD Healthcare Inc., Seoul, Republic of Korea.
Yoon-Keun KimInstitute of MD Healthcare Inc., Seoul, Republic of Korea. ykkim@mdhc.kr.
Korea University · KRResearch & Development Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The relationship between ambient particulate matter exposure and health has been well established. Ultrafine particles (UFP) with a diameter of 100 nm or less are known to increase pulmonary disease risk. Biological factors in dust containing UFP can cause severe inflammatory reactions. Pulmonary diseases develop primarily as a result of chronic inflammation caused by immune dysfunction. Thus, this review focuses on the adverse pulmonary effects of biological UFP, principally lipopolysaccharide (LPS), and bacterial extracellular vesicles (EVs), in indoor dust and the pathophysiological mechanisms involved in the development of chronic pulmonary diseases. The impact of LPS-induced pulmonary inflammation is based primarily on the amount of inhaled LPS. When relatively low levels of LPS are inhaled, a cascade of immune responses leads to Th2 cell induction, and IL-5 and IL-13 released by Th2 cells contributes to asthma development. Conversely, exposure to high levels of LPS induces a Th17 cell response, leading to increased production of IL-17, which is associated with asthma, COPD, and lung cancer incidence. Responses to bacterial EV exposure can similarly be broadly divided based on whether one of two mechanisms, either intracellular or extracellular, is activated, which depends on the type of the parent cell. Extracellular bacteria-derived EVs can cause neutrophilic inflammation via Th17 cell induction, which is associated with asthma, emphysema, COPD, and lung cancer. On the other hand, intracellular bacteria-derived EVs lead to mononuclear inflammation via Th1 cell induction, which increases the risk of emphysema. In conclusion, future measures should focus on the overall reduction of LPS sources in addition to the improvement of the balance of inhaled bacterial EVs in the indoor environment to minimize pulmonary disease risk.

Indexed as

AnimalsBacteriaDustHumansLungParticulate MatterPneumoniaPulmonary EmphysemaTh17 CellsTh1 CellsDustParticulate Matter

Identifiers

PMID32203101
PMCPMC7156658
OpenAlexW3012546753

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.