Rylander R, Holt P G
Department of Environmental Medicine, University of Gothenburg, Sweden.
Mediators Inflamm. 1998;7(2):105-10. doi: 10.1080/09629359891252.
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.
接触灰尘可能涉及同时接触过敏原以及促炎物质。为了研究这种共同接触的影响，在豚鼠吸入T细胞依赖性抗原卵清蛋白（OVA）以及炎症因子（1→3）-β-D-葡聚糖和脂多糖（LPS）的情况下，对其体液和炎症反应进行了研究。通过肺部的炎症细胞和针对OVA的血清抗体来评估这些影响。LPS会刺激OVA诱导的抗体产生，而同时接触（1→3）-β-D-葡聚糖可消除这种刺激。OVA暴露后嗜酸性粒细胞的增加在同时接触（1→3）-β-D-葡聚糖时会减少。结果表明，肺部适应性免疫和先天性免疫机制之间存在复杂的相互作用，这种相互作用由接触空气中灰尘中的常见污染物所决定。
