Department of Agrobioscience, Graduate School of Agricultural Science, Kobe University, 1-1 Rokkodai-cho, Nada-ku, Kobe 657-8501, Japan.
Maruzen Pharmaceuticals Co. Ltd., 1089-8 Sagata, Shinnichi-cho, Fukuyama 729-3102, Japan.
J Biosci Bioeng. 2021 Sep;132(3):271-278. doi: 10.1016/j.jbiosc.2021.05.001. Epub 2021 Jun 1.
In the previous study, pickle-derived Lactiplantibacillus plantarum 22A-3 (LP22A3) suppressed ear edema in passive cutaneous anaphylaxis by its oral administration. Moreover, LP22A3 treatment directly to RBL-2H3 cells shows no effect on β-hexosaminidase release from RBL-2H3 but inhibited its release using the Caco-2/RBL-2H3 cells co-culture system stimulated with LP22A3 from the apical side. In this study, oral administration of LP22A3 decreased total IgE and ovalbumin (OVA) specific IgE contents in blood of BALB/c mice induced food allergy by OVA. Moreover, its oral administration suppressed the development of dermatitis induced by 2,4-dinitrochlorobenzene (DNCB) which was used to develop atopic dermatitis-like lesions in NC/Nga mice. This alleviation was further correlated with a reduction of elevated serum total IgE, transepidermal water loss and elevated acanthosis in the LP22A3-treated group compared with vehicle-treated positive group. In co-culture system composed of Caco-2 and RBL-2H3 cells, LP22A3 treatment on apical side before or after the sensitization with anti-dinitrophenyl (DNP) IgE antibody indicated the different effect on β-hexosaminidase release from RBL-2H3. Its treatment before the sensitization decreased β-hexosaminidase release, but not after sensitization, indicating that LP22A3 affected mast cells sensitized with allergen through intestinal epithelial cells. These results suggest that LP22A3 may have a potential therapeutic property for Type 1 hypersensitivity and atopic dermatitis.
在之前的研究中,泡菜中衍生的植物乳杆菌 22A-3(LP22A3)通过口服给药抑制被动皮肤过敏中的耳部水肿。此外,LP22A3 直接处理 RBL-2H3 细胞对 RBL-2H3 中的β-己糖胺酶释放没有影响,但在 LP22A3 从顶端侧刺激的 Caco-2/RBL-2H3 细胞共培养系统中抑制其释放。在这项研究中,口服 LP22A3 降低了 BALB/c 小鼠食物过敏诱导的血液中总 IgE 和卵清蛋白(OVA)特异性 IgE 含量。此外,其口服给药抑制了 2,4-二硝基氯苯(DNCB)诱导的皮炎的发展,DNCB 用于开发 NC/Nga 小鼠的特应性皮炎样病变。与阳性对照组相比,LP22A3 治疗组血清总 IgE、经皮水分丢失和棘层肥厚升高均降低,这种缓解与升高的总 IgE、经皮水分丢失和棘层肥厚升高的降低进一步相关。在由 Caco-2 和 RBL-2H3 细胞组成的共培养系统中,在用抗二硝基苯基(DNP)IgE 抗体致敏之前或之后在顶端侧处理 LP22A3 对 RBL-2H3 中的β-己糖胺酶释放有不同的影响。致敏前处理降低了β-己糖胺酶的释放,但致敏后不降低,表明 LP22A3 通过肠上皮细胞影响了对过敏原致敏的肥大细胞。这些结果表明 LP22A3 可能对 1 型超敏反应和特应性皮炎具有潜在的治疗特性。