Woon-ki Kim, You Jin Jang, SungJun Park, Sung-gyu Min, Heeun Kwon, Min Jung Jo, GwangPyo Ko
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引用次数: 0
摘要
特应性皮炎(AD)是一种慢性炎症性皮肤病,会反复加重湿疹和瘙痒。益生菌可通过调节免疫反应和肠道微生物群来预防或治疗特应性皮炎。在本研究中,我们使用屋尘螨(Dermatophagoides farinae)诱导的体内 AD 模型评估了嗜酸乳杆菌(L. acidophilus)KBL409 的作用。口服嗜酸乳杆菌 KBL409 能显著降低皮炎评分,减少皮肤组织中免疫细胞的浸润。嗜酸乳杆菌 KBL409 能降低血清免疫球蛋白 E 和皮肤组织中 T 辅助细胞(Th)1(干扰素-γ)、Th2(白细胞介素 [IL]-4、IL-5、IL-13 和 IL-31)和 Th17(IL-17A)细胞因子的 mRNA 水平。在嗜酸乳杆菌 KBL409 诱导的 AD 诱导的小鼠中,抗炎细胞因子 IL-10 增加,Foxp3 表达上调。此外,嗜酸乳杆菌 KBL409 还能显著调节肠道微生物群以及短链脂肪酸和氨基酸的浓度,这可以解释其对 AD 的影响。我们的研究结果表明,嗜酸乳杆菌KBL409可通过调节宿主的免疫反应和肠道微生物群来治疗AD。
Lactobacillus acidophilus KBL409 Ameliorates Atopic Dermatitis in a Mouse Model
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.
期刊介绍:
Publishes papers that deal with research on microorganisms, including archaea, bacteria, yeasts, fungi, microalgae, protozoa, and simple eukaryotic microorganisms. Topics considered for publication include Microbial Systematics, Evolutionary Microbiology, Microbial Ecology, Environmental Microbiology, Microbial Genetics, Genomics, Molecular Biology, Microbial Physiology, Biochemistry, Microbial Pathogenesis, Host-Microbe Interaction, Systems Microbiology, Synthetic Microbiology, Bioinformatics and Virology. Manuscripts dealing with simple identification of microorganism(s), cloning of a known gene and its expression in a microbial host, and clinical statistics will not be considered for publication by JM.