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首页> 外文期刊>Infection and immunity >Intranasal Exposure to Bacterial Superantigens Induces Airway Inflammation in HLA Class II Transgenic Mice
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Intranasal Exposure to Bacterial Superantigens Induces Airway Inflammation in HLA Class II Transgenic Mice

机译：鼻内暴露于细菌超抗原可诱导HLA II类转基因小鼠气道炎症

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Staphylococcus aureus is widely prevalent in the nasopharynges of healthy individuals (carriers) but can also cause serious infections. S. aureus can elaborate a variety of superantigen exotoxins in “carrier” or “pathogenic” states. Streptococcus pyogenes can also colonize the nasopharynx and elaborate superantigens. Unlike the acute effects of superantigen exotoxins absorbed through the gut or vaginal mucosa, little is known regarding the pathogenesis of superantigens entering through the intranasal route. In the current study, we evaluated the local and systemic effects of staphylococcal enterotoxin B (SEB) and streptococcal pyrogenic exotoxin A (SPEA) delivered through the intranasal route. Superantigens were administered intranasally on multiple occasions, and experimental animals were sacrificed on day 8 for experimental analyses. SEB-induced airway inflammation was more pronounced for HLA-DR3 transgenic mice than for BALB/c mice, consistent with bacterial superantigens binding more efficiently to human than murine major histocompatibility complex class II. The nature of the airway inflammation in HLA-DR3 mice was determined by the concentration of SEB applied intranasally. Low concentrations (20 ng) induced eosinophilic airway inflammation as well as eosinophil degranulation, whereas intranasal exposure to higher concentrations (2,000 ng) resulted in neutrophilic airway inflammation, permanent airway destruction, toxic shock, and mortality. SEB-induced eosinophilic inflammatory response was enhanced in signal transducer and activator of transcription (STAT)-4-deficient HLA-DQ8 transgenic mice with defective interleukin-12 signaling. Intranasal administration of SPEA induced airway inflammation and systemic immune activation in HLA-DQ8 transgenic mice. In conclusion, repeated chronic intranasal exposure to bacterial superantigens causes airway inflammation and systemic immune activation.
机译：金黄色葡萄球菌在健康个体（携带者）的鼻咽中广泛流行，但也会引起严重的感染。 S。金黄色葡萄球菌可以修饰多种“抗原”或“致病”状态的超抗原外毒素。化脓性链球菌也可以在鼻咽中定殖并形成超抗原。与通过肠或阴道粘膜吸收的超抗原外毒素的急性作用不同，对于通过鼻内途径进入的超抗原的发病机理知之甚少。在本研究中，我们评估了通过鼻内途径递送的葡萄球菌肠毒素B（SEB）和链球菌热原性外毒素A（SPEA）的局部和全身作用。多次鼻内给予超抗原，并在第8天处死实验动物进行实验分析。 SEB诱导的气道炎症对于HLA-DR3转基因小鼠比对BALB / c小鼠更为明显，这与细菌超抗原对人类的结合要比对鼠类主要组织相容性复合物II类更为有效。 HLA-DR3小鼠气道炎症的性质取决于鼻内应用SEB的浓度。低浓度（20 ng）会诱发嗜酸性气道炎症以及嗜酸性粒细胞脱颗粒，而鼻内暴露于较高浓度（2,000 ng）会导致嗜中性气道炎症，永久性气道破坏，中毒性休克和死亡率。 SEB诱导的嗜酸性粒细胞炎症反应在白介素12信号缺陷的信号转导和转录激活（STAT）-4缺陷型HLA-DQ8转基因小鼠中得到增强。在HLA-DQ8转基因小鼠中，SPEA的鼻内给药可引起气道炎症和全身免疫激活。总之，反复长期鼻内暴露于细菌超抗原会导致气道炎症和全身免疫激活。

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