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. 2024 Feb;62(2):91-99.
doi: 10.1007/s12275-024-00104-5. Epub 2024 Feb 22.

Lactobacillus acidophilus KBL409 Ameliorates Atopic Dermatitis in a Mouse Model

Affiliations

Lactobacillus acidophilus KBL409 Ameliorates Atopic Dermatitis in a Mouse Model

Woon-Ki Kim et al. J Microbiol. 2024 Feb.

Abstract

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.

Keywords: Lactobacillus acidophilus; Atopic dermatitis; Gut-skin axis; Immune response; Microbiota; Probiotic.

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Conflict of interest statement

G.K. is the founder of KoBioLabs, Inc, and S.P. is an employee of KoBioLabs, Inc. The other authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Fig. 1
Fig. 1
Effects of L. acidophilus KBL409 on AD symptoms. A Skin samples stained with hematoxylin and eosin; B Dermatitis score; C Serum IgE concentration. When appropriate, data are suggested as the mean ± standard deviation (SD) of experimental groups (nine mice per each group). Asterisks indicate a statistically significance (*P < 0.05; ***P < 0.001; the Mann–Whitney U test compared to the DFE + PBS-treated group)
Fig. 2
Fig. 2
Effects of L. acidophilus KBL409 on mRNA levels of cytokines and Foxp3 in AD-induced mice. Data are suggested as the mean ± SD of three independent experiments. Asterisks indicate a statistically significance (*P < 0.05; **P < 0.01; ***P < 0.001; the Mann–Whitney U test compared to the DFE + PBS-treated group)
Fig. 3
Fig. 3
Effects of L. acidophilus KBL409 on cecal microbiota in AD-induced mice. A Shannon diversity indices; B Plots of the Bray–Curtis dissimilarity distance-based principal coordinates analyses; C Taxonomic structures of cecal microbiome in experimental groups; D Comparisons of significantly different taxa in experimental groups determined by LEfSe analyses (threshold > 2.5)
Fig. 4
Fig. 4
Effects of L. acidophilus KBL409 on predicted metabolic pathways and metabolite concentrations in cecum of AD-induced mice. A Predicted metabolic pathways determined by PICRUSt2 analyses; B Butyrate and propionate; C Aspartic acid and threonine. When appropriate, data are suggested as the mean ± SD of three independent experiments. Asterisks indicate a statistically significance (*P < 0.05; **P < 0.01; ***P < 0.001; the Mann–Whitney U test compared to the DFE + PBS-treated group)

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