Lactobacillus acidophilus KBL409 Ameliorates Atopic Dermatitis in a Mouse Model.
Atopic dermatitis
Gut-skin axis
Immune response
Lactobacillus acidophilus
Microbiota
Probiotic
Journal
Journal of microbiology (Seoul, Korea)
ISSN: 1976-3794
Titre abrégé: J Microbiol
Pays: Korea (South)
ID NLM: 9703165
Informations de publication
Date de publication:
22 Feb 2024
22 Feb 2024
Historique:
received:
20
08
2023
accepted:
27
12
2023
revised:
11
12
2023
medline:
22
2
2024
pubmed:
22
2
2024
entrez:
22
2
2024
Statut:
aheadofprint
Résumé
Atopic dermatitis (AD) is a chronic inflammatory skin disease with repeated exacerbations of eczema and pruritus. Probiotics can prevent or treat AD appropriately via modulation of immune responses and gut microbiota. In this study, we evaluated effects of Lactobacillus acidophilus (L. acidophilus) KBL409 using a house dust mite (Dermatophagoides farinae)-induced in vivo AD model. Oral administration of L. acidophilus KBL409 significantly reduced dermatitis scores and decreased infiltration of immune cells in skin tissues. L. acidophilus KBL409 reduced in serum immunoglobulin E and mRNA levels of T helper (Th)1 (Interferon-γ), Th2 (Interleukin [IL]-4, IL-5, IL-13, and IL-31), and Th17 (IL-17A) cytokines in skin tissues. The anti-inflammatory cytokine IL-10 was increased and Foxp3 expression was up-regulated in AD-induced mice with L. acidophilus KBL409. Furthermore, L. acidophilus KBL409 significantly modulated gut microbiota and concentrations of short-chain fatty acids and amino acids, which could explain its effects on AD. Our results suggest that L. acidophilus KBL409 is the potential probiotic for AD treatment by modulating of immune responses and gut microbiota of host.
Identifiants
pubmed: 38386273
doi: 10.1007/s12275-024-00104-5
pii: 10.1007/s12275-024-00104-5
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : National Research Foundation of Korea
ID : NRF-2021R1I1A1A01048923
Organisme : National Research Foundation of Korea
ID : NRF-2022M3A9F3017371
Organisme : National Research Foundation of Korea
ID : NRF-2022M3A9F3017371
Organisme : National Research Foundation of Korea
ID : NRF-2022M3A9F3017371
Organisme : National Research Foundation of Korea
ID : NRF-2022M3A9F3017371
Organisme : National Research Foundation of Korea
ID : NRF-2022M3A9F3017371
Organisme : National Research Foundation of Korea
ID : NRF-2022M3A9F3017371
Organisme : National Research Foundation of Korea
ID : NRF-2022M3A9F3017371
Informations de copyright
© 2024. The Author(s).
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