Evidence map›Paper›PMID 36684665›Full record

ArticlePeerJ2023

Solithromycin inhibits IL-13-induced goblet cell hyperplasia and MUC5AC, CLCA1, and ANO1 in human bronchial epithelial cells.

Yasuhiro Kimura, Masahiro Shinoda, Masaharu Shinkai, Takeshi Kaneko

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PeerJ, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. 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.

Yasuhiro KimuraDepartment of Pulmonology, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.
Masahiro ShinodaDepartment of Respiratory Medicine, Tokyo Shinagawa Hospital, Shinagawa, Tokyo, Japan.
Masaharu ShinkaiDepartment of Respiratory Medicine, Tokyo Shinagawa Hospital, Shinagawa, Tokyo, Japan.
Takeshi KanekoDepartment of Pulmonology, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.
New Tokyo Hospital · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Solithromycin is a novel fluoroketolide antibiotic belonging to the class of macrolide antibiotics. Activation of the interleukin (IL)-13 receptor leads to STAT6 activation and subsequent induction of SAM pointed domain containing ETS transcription factor (SPDEF), chloride channel accessory 1 (CLCA1), and anoctamin-1 (ANO1), all of which are associated with the induction of MUC5AC. We examined the effects of solithromycin on mucin production led by IL-13 signaling. Normal human bronchial epithelial cells were grown at the air-liquid interface with IL-13 with/without solithromycin for 14 days. Histochemical analysis was performed using hematoxylin and eosin staining and MUC5AC immunostaining.

Indexed as

Goblet CellsInterleukin-13MacrolidesAnoctamin-1Chloride ChannelsHumansHyperplasiaMucin 5ACNeoplasm ProteinsRNA, MessengerTriazolesANO1 protein, humanAnoctamin-1Chloride ChannelsCLCA1 protein, humanInterleukin-13MacrolidesMUC5AC protein, humanMucin 5ACNeoplasm ProteinsRNA, MessengersolithromycinTriazolesAnoctamin-1Chloride channel accessory 1Goblet cellMUC5ACMucinSAM pointed domain containing ETS transcription factorSolithromycin

Identifiers

PMID36684665
PMCPMC9854378
OpenAlexW4316673551

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.