Staphylococcus aureus from atopic dermatitis skin accumulates in the lysosomes of keratinocytes with induction of IL-1α secretion via TLR9.
Biomarkers
Cell Line
Cytokines
/ metabolism
Dermatitis, Atopic
/ diagnosis
Humans
Interleukin-1alpha
/ metabolism
Keratinocytes
/ immunology
Lysosomes
/ metabolism
Phagocytosis
/ immunology
Signal Transduction
Staphylococcal Infections
/ complications
Staphylococcus aureus
/ immunology
Toll-Like Receptor 9
/ genetics
atopic dermatitis
dermatology
innate immunity
microbiome
staphylococcus aureus
Journal
Allergy
ISSN: 1398-9995
Titre abrégé: Allergy
Pays: Denmark
ID NLM: 7804028
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
29
04
2018
revised:
22
08
2018
accepted:
30
08
2018
pubmed:
1
10
2018
medline:
18
4
2020
entrez:
1
10
2018
Statut:
ppublish
Résumé
Staphylococcus aureus (S. aureus) is frequently detected in the skin of patients with atopic dermatitis (AD), and involved in the flare of AD. There are some evidence-specific strains of S. aureus affect the severity of AD. However, the mechanism of predominant colonization and the aggravation of dermatitis by certain strains of S. aureus in the patients with AD are still unknown. To reveal the characteristics of S. aureus from patients with AD (S. aureus-AD), we analyzed the interaction of S. aureus-AD and keratinocytes in comparison with those of S. aureus laboratory strains (S. aureus-stand.). We stimulated HaCaT cells, keratinocyte cell line, and human epidermal keratinocytes by heat-killed S. aureus strains, then evaluated immune response of keratinocytes by ELISA, immunofluorescence staining, and flow cytometry. Upon incubation with keratinocytes, three out of four strains of heat-killed S. aureus-AD were strongly agglutinated inside the cytoplasm. In the cells, they are located in lysosomes and promoted the secretion of interleukin-1α (IL-1α). These reactions were not observed by any of four strains of S. aureus-stand. and S. epidermidis and were abolished by the treatment of S. aureus with proteinase K. Moreover, the IL-1α secretion was diminished by the inhibition of Toll-like receptor 9 (TLR9). S. aureus-AD accumulates in lysosome of keratinocytes by means of bacterial cell wall proteins and induces IL-1α via TLR9.
Sections du résumé
BACKGROUND
Staphylococcus aureus (S. aureus) is frequently detected in the skin of patients with atopic dermatitis (AD), and involved in the flare of AD. There are some evidence-specific strains of S. aureus affect the severity of AD. However, the mechanism of predominant colonization and the aggravation of dermatitis by certain strains of S. aureus in the patients with AD are still unknown.
OBJECTIVE
To reveal the characteristics of S. aureus from patients with AD (S. aureus-AD), we analyzed the interaction of S. aureus-AD and keratinocytes in comparison with those of S. aureus laboratory strains (S. aureus-stand.).
METHODS
We stimulated HaCaT cells, keratinocyte cell line, and human epidermal keratinocytes by heat-killed S. aureus strains, then evaluated immune response of keratinocytes by ELISA, immunofluorescence staining, and flow cytometry.
RESULTS
Upon incubation with keratinocytes, three out of four strains of heat-killed S. aureus-AD were strongly agglutinated inside the cytoplasm. In the cells, they are located in lysosomes and promoted the secretion of interleukin-1α (IL-1α). These reactions were not observed by any of four strains of S. aureus-stand. and S. epidermidis and were abolished by the treatment of S. aureus with proteinase K. Moreover, the IL-1α secretion was diminished by the inhibition of Toll-like receptor 9 (TLR9).
CONCLUSION
S. aureus-AD accumulates in lysosome of keratinocytes by means of bacterial cell wall proteins and induces IL-1α via TLR9.
Substances chimiques
Biomarkers
0
Cytokines
0
IL1A protein, human
0
Interleukin-1alpha
0
TLR9 protein, human
0
Toll-Like Receptor 9
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
560-571Subventions
Organisme : JSPS KAKENHI
ID : 15H06428
Pays : International
Organisme : JSPS KAKENHI
ID : 18K16031
Pays : International
Organisme : GlaxoSmithKline Japan research grant
ID : B-26
Pays : International
Organisme : Mitsubishi Tanabe Pharma Research Grant
ID : MTPS20170515014
Pays : International
Informations de copyright
© 2018 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd.