胸腺基质淋巴细胞生成素
金黄色葡萄球菌
细胞因子
医学
鼻息肉
免疫学
超抗原
免疫系统
促炎细胞因子
Toll样受体
炎症
T细胞
微生物学
生物
先天免疫系统
细菌
遗传学
作者
Feng Lan,Nan Zhang,Gabriele Holtappels,Natalie De Ruyck,Olga Krysko,Koen Van Crombruggen,Harald Braun,Sebastian L. Johnston,Nikos T. Papadopoulos,Luo Zhang,Claus Bachert
标识
DOI:10.1164/rccm.201710-2112oc
摘要
Chronic rhinosinusitis with nasal polyps is characterized by a T-helper cell type 2-skewed upper airway inflammation. Mucosal Staphylococcus aureus colonization is found in the majority of patients with nasal polyps. S. aureus is known to induce type 2 cytokine release via enterotoxins.To investigate the impact of non-enterotoxin-producing S. aureus on type 2 cytokine release.TSLP (thymic stromal lymphopoietin), IL-33, and type 2 cytokines were assessed in a human mucosal tissue model upon S. aureus infection.S. aureus exposure increased the expression of IL-33, TSLP, IL-5, and IL-13 in nasal polyp tissue, accompanied by elevated expression levels of TSLP and IL-33 receptors, predominantly on CD3+ T cells. S. aureus infection led to the release of TSLP, but not IL-33, IL-5, or IL-13, from healthy inferior turbinate tissue. In contrast, S. epidermidis did not induce any epithelial cell-derived cytokines in nasal polyp or healthy tissue. S. aureus infection also increased the release of IL-33 and TSLP in BEAS-2B epithelial cells, accompanied by activation of NF-κB (nuclear factor κB) pathways. Incubation with CU-CPT22, a specific Toll-like receptor 2 antagonist, significantly reduced the S. aureus-induced release of TSLP and IL-33, and the activity of the NF-κB signal in BEAS-2B cells.This study demonstrates for the first time that S. aureus can directly induce epithelial cell-derived cytokine release via binding to Toll-like receptor 2, and may thereby propagate type 2 cytokine expression in nasal polyp tissue.
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