We previously reported that Asian sand dust (ASD), which contains particulate matter (PM) less than 10 μm in diameter (PM10), induced subacute inflammation in splenocytes. However, it was unclear whether the PM itself or compounds attached to its surface induced the inflammation. Here we characterized the role of organic substances adsorbed onto the PM10 surface in triggering inflammation by comparing the effect on splenocyte activation of PM10 from urban areas (urPM10), which is rich in lipopolysaccharide (LPS) as compared to ASD, with that of heated PM10 (H-PM). BALB/c mice were intratracheally administered urPM10 or H-PM with or without LPS (1 ng and 10 ng) four times at 2-week intervals, and splenocytes were prepared at 24 h after the final administration to assay the immune responses. urPM10 suppressed splenocyte activation, while H-PM activated splenocytes and LPS neutralization by polymyxin B rescued urPM10-induced immunosuppression. Co-administration of LPS with H-PM clearly suppressed mitogen-induced immune responses in the spleen. Consistent with these results, H-PM induced the phosphorylation of nuclear factor κB (NF-κB) p65 and I kappa B kinase (IKK), which was inhibited by co-administration of LPS. In mice deficient in the LPS signal transducer MyD88, splenocyte activation after LPS or H-PM treatment in vivo was comparable to that in the control. Altogether, our results indicate that PM10 itself could activate NF-κB through the MyD88 pathway, which was modulated by the amount of LPS attached.

中文翻译：

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附着在城市颗粒物10上的脂多糖抑制脾细胞的免疫反应，而颗粒物本身激活NF-κB。

我们之前曾报道过，亚洲沙尘（ASD）包含直径小于10μm（PM10）的颗粒物（PM），可引起脾细胞亚急性炎症。但是，尚不清楚PM本身或附着在其表面的化合物是否会引起炎症。在这里，我们通过比较城市地区PM10的脾细胞活化作用（urPM10）（与ASD相比富含脂多糖（LPS））与加热的PM10对脾脏激活PM10的作用，来表征吸附在PM10表面的有机物质在触发炎症中的作用。 （H-PM）。对BALB / c小鼠每2周间隔气管内施用urPM10或H-PM含或不含LPS（1 ng和10 ng）四次，最后一次给药后24小时准备脾细胞以测定免疫反应。urPM10抑制脾细胞活化，H-PM激活的脾细胞和多粘菌素B对LPS的中和作用挽救了urPM10诱导的免疫抑制。LPS与H-PM的共同给药可明显抑制脾中丝裂原诱导的免疫反应。与这些结果一致，H-PM诱导了核因子κB（NF-κB）p65和IκB激酶（IKK）的磷酸化，这被LPS的共同给药所抑制。在缺乏LPS信号转导器MyD88的小鼠中，体内LPS或H-PM处理后的脾细胞活化与对照组相当。总之，我们的结果表明，PM10本身可以通过MyD88途径激活NF-κB，该途径受LPS附着量的调节。LPS与H-PM的共同给药可明显抑制脾中丝裂原诱导的免疫反应。与这些结果一致，H-PM诱导了核因子κB（NF-κB）p65和IκB激酶（IKK）的磷酸化，这被LPS的共同给药所抑制。在缺乏LPS信号转导器MyD88的小鼠中，体内LPS或H-PM处理后的脾细胞活化与对照组相当。总之，我们的结果表明，PM10本身可以通过MyD88途径激活NF-κB，该途径受LPS附着量的调节。LPS与H-PM的共同给药可明显抑制脾中丝裂原诱导的免疫反应。与这些结果一致，H-PM诱导了核因子κB（NF-κB）p65和IκB激酶（IKK）的磷酸化，这被LPS的共同给药所抑制。在缺乏LPS信号转导器MyD88的小鼠中，体内LPS或H-PM处理后的脾细胞活化与对照组相当。总之，我们的结果表明，PM10本身可以通过MyD88途径激活NF-κB，该途径受LPS附着量的调节。体内LPS或H-PM处理后，脾细胞活化与对照组相当。总之，我们的结果表明，PM10本身可以通过MyD88途径激活NF-κB，该途径受LPS附着量的调节。体内LPS或H-PM处理后，脾细胞活化与对照组相当。总之，我们的结果表明，PM10本身可以通过MyD88途径激活NF-κB，该途径受LPS附着量的调节。