Hierarchically ordered mesocellular mesoporous silica materials (HMMS) were synthesized using a single structure-directing agent. The mesocellular pores are synthesized without adding any pore expander; the pore walls are composed of SBA-15 type mesopores. Small-angle X-ray scattering revealed the presence of uniform pore structures with two different sizes. Using HMMS as a nanoscopic template, hierarchically ordered mesocellular mesoporous carbon (HMMC) and polymer (HMMP) materials were synthesized. HMMS was used as a host for enzyme immobilization. To improve the retention of enzymes in HMMS, we adsorbed enzymes, and then employed crosslinking using glutaraldehyde (GA). The resulting crosslinked enzyme aggregates (CLEAs) show an impressive stability with extremely high enzyme loadings. For example, 0.5 g alpha-chymotrypsin (CT) could be loaded in 1 g of silica with no activity decrease observed with rigorous shaking over one month. In contrast, adsorbed CT without GA treatment resulted in a lower loading, which further decreased due to continuous leaching of adsorbed CT under shaking. The activity of crosslinked CT aggregates in HMMS was approximately 10 times higher than that of the adsorbed CT, which represents a 74-fold increase in activity per unit weight of HMMS due to higher CT loading.

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Peroxisome proliferator-activated receptor ␥ (PPAR␥) plays an important role in controlling immune and inflammatory responses. Recent studies have demonstrated that activation of PPAR␥ reduces airway hyper-responsiveness and activation of eosinophils that are increased by induction of asthma. We have used a mouse model of asthma to determine the role of PPAR␥ in the regulation of the pulmonary immune response, more specifically in the involvement of immunoregulatory cytokine interleukin (IL)-10. Administration of PPAR␥ agonists or adenovirus carrying PPAR␥ cDNA (AdPPAR␥) reduced eosinophilic airway inflammation and airway hyper-responsiveness. Expression of PPAR␥ was increased by ovalbumin inhalation, and the increase was further enhanced by the administration of PPAR␥ agonists or AdPPAR␥. The increased IL-10 levels in lung tissues after ovalbumin inhalation were further increased by the administration of rosiglitazone, pioglitazone, or AdPPAR␥. Levels of IL-4, IL-5, and ovalbumin-specific IgE were also increased after ovalbumin inhalation, and the increased levels were significantly reduced by the administration of the PPAR␥ agonists or AdPPAR␥. The results also showed that inhibition of IL-10 activity with anti-IL-10 receptor antibody partially restored the inflammation. These findings suggest that a protective role of PPAR␥ in the pathogenesis of the asthma is partly mediated through an IL-10-dependent mechanism.