Department of Otorhinolaryngology, Gyeongsang National University Hospital, Jinju, Republic of Korea.
Department of Otorhinolaryngology - Head and Neck Surgery, Seoul National University College of Medicine, 103, Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea.
BMC Microbiol. 2020 Oct 7;20(1):301. doi: 10.1186/s12866-020-01974-6.
The host-microbial commensalism can shape the innate immune responses in respiratory mucosa and nasal microbiome also modulates front-line immune mechanism in the nasal mucosa. Inhaled allergens encounter the host immune system first in the nasal mucosa, and microbial characteristics of nasal mucus directly impact the mechanisms of initial allergic responses in nasal epithelium. However, the roles of the nasal microbiome in allergic nasal mucosa remain uncertain. We sought to determine the distribution of nasal microbiomes in allergic nasal mucosa and elucidate the interplay between nasal microbiome Staphylococcus species and Th2 cytokines in allergic rhinitis (AR) models.
Staphylococcus aureus (AR-SA) and S. epidermidis (AR-SE) were isolated from the nasal mucosa of patients with AR. The influence of nasal microbiome Staphylococcus species on allergic nasal mucosa was also tested with in vitro and in vivo AR models. Pyrosequencing data showed that colonization by S. epidermidis and S. aureus was more dominant in nasal mucus of AR subjects. The mRNA and protein levels of IL-33 and TSLP were significantly higher in AR nasal epithelial (ARNE) cells which were cultured from nasal mucosa of AR subjects, and exposure of ARNE cells to AR-SA reduced IL-33 mRNA and secreted protein levels. Particularly, ovalbumin-driven AR mice inoculated with AR-SA by intranasal delivery exhibited significantly reduced IL-33 in their nasal mucosa. In the context of these results, allergic symptoms and Th2 cytokine levels were significantly downregulated after intranasal inoculation of AR-SA in vivo AR mice.
Colonization by Staphylococcus species was more dominant in allergic nasal mucosa, and nasal commensal S. aureus from subjects with AR mediates anti-allergic effects by modulating IL-33-dependent Th2 inflammation. The results demonstrate the role of host-bacterial commensalism in shaping human allergic inflammation.
宿主-微生物共生关系可以影响呼吸道黏膜的固有免疫反应，鼻腔微生物组也调节鼻腔黏膜的一线免疫机制。吸入性过敏原首先在鼻腔黏膜中遇到宿主免疫系统，鼻腔黏液中的微生物特征直接影响鼻上皮初始过敏反应的机制。然而，鼻腔微生物组在变应性鼻黏膜中的作用尚不确定。我们试图确定变应性鼻黏膜中鼻腔微生物组的分布，并阐明变应性鼻炎（AR）模型中鼻腔微生物组葡萄球菌种与 Th2 细胞因子之间的相互作用。
从 AR 患者的鼻腔黏膜中分离出金黄色葡萄球菌（AR-SA）和表皮葡萄球菌（AR-SE）。还通过体外和体内 AR 模型测试了鼻腔微生物组葡萄球菌种对变应性鼻黏膜的影响。焦磷酸测序数据显示，表皮葡萄球菌和金黄色葡萄球菌的定植在 AR 患者的鼻腔黏液中更为占优势。从 AR 患者鼻腔黏膜培养的 AR 鼻上皮（ARNE）细胞中，IL-33 和 TSLP 的 mRNA 和蛋白水平明显升高，暴露于 AR-SA 可降低 IL-33 mRNA 和分泌蛋白水平。特别是，卵清蛋白驱动的 AR 小鼠经鼻腔内接种 AR-SA 后，其鼻腔黏膜中 IL-33 明显减少。在这些结果的背景下，AR 小鼠体内经鼻腔接种 AR-SA 后，过敏症状和 Th2 细胞因子水平明显下调。
葡萄球菌种的定植在变应性鼻黏膜中更为占优势，来自 AR 患者的鼻腔共生金黄色葡萄球菌通过调节 IL-33 依赖性 Th2 炎症介导抗过敏作用。结果表明宿主-细菌共生关系在塑造人类过敏炎症中的作用。
