Evidence map›Paper›PMID 26438797›Full record

ArticleInfection and immunity2015

Pathophysiological changes induced by Pseudomonas aeruginosa infection are involved in MMP-12 and MMP-13 upregulation in human carcinoma epithelial cells and a pneumonia mouse model.

Ji-Won Park, In-Sik Shin, Un-Hwan Ha, Sei-Ryang Oh, Jae-Hong Kim, Kyung-Seop Ahn

Open access · hybridAbstract read
In one paragraph

Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Frontiers in cellular and infection microbiology · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. NOX4 MediatesAntioxidants (Basel, Switzerland) · 2021
    Article
  9. Article
  10. 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 3 institutions in 1 country.

Ji-Won ParkNatural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Chungbuk, Republic of Korea College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
In-Sik ShinCollege of Veterinary Medicine, Chonnam National University, Gwangju, Republic of Korea.
Un-Hwan HaDepartment of Biotechnology and Bioinformatics, Korea University, Sejong, Republic of Korea.
Sei-Ryang OhNatural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Chungbuk, Republic of Korea.
Jae-Hong KimCollege of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea jhongkim@korea.ac.kr ksahn@kribb.re.kr.
Kyung-Seop AhnNatural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Chungbuk, Republic of Korea jhongkim@korea.ac.kr ksahn@kribb.re.kr.
Korea Research Institute of Bioscience and Biotechnology · KRKorea University · KRChonnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudomonas aeruginosa infections persist in patients with cystic fibrosis (CF) and drive lung disease progression. P. aeruginosa potently activates the innate immune system mostly through the recognition of pathogen-associated molecular patterns, such as flagellin. Matrix metalloproteinases 12 and 13 (MMP-12 and MMP-13, respectively) exacerbate chronic lung infection and inflammation by promoting uncontrolled tissue rearrangements and fibrosis, yet the underlying molecular mechanisms by which this occurs remain largely unknown. In this study, we used quantitative bacteriology, histological examination, and proinflammatory cytokine levels to evaluate the effects of MMP-12 and MMP-13 on P. aeruginosa strain K-induced infection and pneumonia in H292 epithelial cells and mice, respectively. Under inflammatory stimulation, mRNA and protein expression levels of proinflammatory mediators were higher in strain K-infected mice and cells than in uninfected counterparts, in which MMP-12 and MMP-13 expression reached levels similar to those observed in epithelial cells. Moreover, we also found that the NF-κB pathway might be involved in the induction of cytokines in response to strain K infection. Taken together, these data suggest that MMP-12 and MMP-13 alter strain K infection in mice and play a role in inflammatory regulation by modulating cytokine levels.

Indexed as

AnimalsCell Line, TumorCystic FibrosisCytokinesDisease Models, AnimalEpithelial CellsFemaleGene Expression RegulationHost-Pathogen InteractionsHumansImmunity, InnateMatrix Metalloproteinase 12Matrix Metalloproteinase 13MiceMice, Inbred C57BLNF-kappa BCytokinesmatrix metallopeptidase 12, mouseMatrix Metalloproteinase 12Matrix Metalloproteinase 13NF-kappa B

Identifiers

PMID26438797
PMCPMC4645383
OpenAlexW2180821495

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.