Methods: Three types of SNPs were used: spherical SNPs (S-SNPs), mesoporous SNPs (M-SNPs), and PEGylated SNPs (P-SNPs). In the acute SNP exposure model performed, six-week-old BALB/c female mice were intranasally inoculated with SNPs for 3 consecutive days. In the OVA/SNPs asthma model, the mice were sensitized two times via the peritoneal route with OVA. Additionally, the mice endured OVA with or without SNP challenges intranasally.
Results: Acute SNP exposure induced significant airway inflammation and AHR, particularly in the S-SNPs group. In OVA/SNPs asthma models, OVA with SNPs treated group showed significant airway inflammation, more than those treated with only OVA and without SNPs. In these models, the P-SNPs group induced lower levels of inflammation on airways than both the S-SNPs or M-SNPs groups. Interleukin (IL)-5, IL-13, IL-1β, and interferon-gamma (IFN-γ) levels correlated with airway inflammation in the tested models, without statistical significance.
Conclusions: In the mouse models studied, increased airway inflammation was associated with acute SNPs exposure, whether exposed solely to SNPs or SNPs in conjunction with OVA. P-SNPs appear to be relatively safer for clinical use than S-SNPs and M-SNPs, as determined by lower observed toxicity and airway system inflammation.