Lipopolysaccharide attached to urban particulate matter 10 suppresses immune responses in splenocytes while particulate matter itself activates NF-κB.

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.