Solithromycin inhibits IL-13-induced goblet cell hyperplasia and MUC5AC, CLCA1, and ANO1 in human bronchial epithelial cells.
Anoctamin-1
Chloride channel accessory 1
Goblet cell
MUC5AC
Mucin
SAM pointed domain containing ETS transcription factor
Solithromycin
Journal
PeerJ
ISSN: 2167-8359
Titre abrégé: PeerJ
Pays: United States
ID NLM: 101603425
Informations de publication
Date de publication:
2023
2023
Historique:
received:
12
07
2022
accepted:
14
12
2022
entrez:
23
1
2023
pubmed:
24
1
2023
medline:
25
1
2023
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 36684665
doi: 10.7717/peerj.14695
pii: 14695
pmc: PMC9854378
doi:
Substances chimiques
ANO1 protein, human
0
Anoctamin-1
0
Chloride Channels
0
CLCA1 protein, human
0
Interleukin-13
0
Macrolides
0
MUC5AC protein, human
0
Mucin 5AC
0
Neoplasm Proteins
0
RNA, Messenger
0
solithromycin
9U1ETH79CK
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e14695Informations de copyright
©2023 Kimura et al.
Déclaration de conflit d'intérêts
The authors declare there are no competing interests.
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