首页> 美国卫生研究院文献>Mediators of Inflammation >(1--3)-beta-D-glucan and endotoxin modulate immune response to inhaled allergen.
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(1--3)-beta-D-glucan and endotoxin modulate immune response to inhaled allergen.

机译:(1- 3)-β-D-葡聚糖和内毒素调节对吸入变应原的免疫反应。

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摘要

Exposure to dust may involve co-exposure to agents which are allergens, together with those which are pro-inflammatory. To study the effects of such a co-exposure, the humoral and inflammatory responses were studied in guinea pigs inhaling the T-cell-dependent antigen ovalbumin (OVA) and the inflammatory agents (1 --> 3)-beta-D-glucan and lipopolysaccharide (LPS). The effects were evaluated as inflammatory cells in the lung and serum antibodies to OVA. LPS caused a stimulation of the OVA-induced antibody production which was abolished by simultaneous exposure to (1 --> 3)-beta-D-glucan. An increase of eosinophils after OVA exposure was decreased by co-exposure to (1 --> 3)-beta-D-glucan. The results demonstrate a complex interaction between adaptive and innate immune mechanisms in the lung, determined by exposure to common contaminants in airborne dust.
机译:接触粉尘可能涉及同时接触过敏原和促炎剂。为了研究这种共同暴露的影响,研究了豚鼠吸入T细胞依赖性抗原卵清蛋白(OVA)和炎性药物(1-> 3)-β-D-葡聚糖时的体液和炎症反应和脂多糖(LPS)。以肺中的炎性细胞和OVA的血清抗体来评估作用。 LPS刺激了OVA诱导的抗体生成,但同时暴露于(1-> 3)-β-D-葡聚糖可消除这种刺激。共同暴露于(1-> 3)-β-D-葡聚糖可减少OVA暴露后嗜酸性粒细胞的增加。结果表明,肺部适应性免疫机制与先天免疫机制之间存在复杂的相互作用,这取决于暴露于空气中粉尘中的常见污染物。

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