Background Allergic asthma is a major global health concern owing to its high prevalence and substantial socioeconomic burden. It is characterized by elevated levels of immunoglobulin E (IgE), which plays a pivotal role in the pathophysiology of allergic disorders. Therapeutic anti-IgE antibodies, including omalizumab, have emerged as a validated strategy for the management of IgE-mediated disorders. However, their clinical use requires repeated administration and remains costly. Here, we developed a nanoparticle-based anti-IgE vaccine by genetically fusing an IgE-derived epitope peptide to the N-terminus of a hybrid ferritin. Results The antigen was expressed in E.coli and purified to homogeneity. Preventive vaccination was conducted in a mouse model of chronic allergic asthma. High levels of anti-IgE antibodies were elicited and ameliorated key features of allergic asthma including the reduction in IgE levels, peribronchiolar inflammation, mucus production, and altered expression of inflammation-related genes. Conclusion The anti-IgE vaccine developed in this study has protective effects in allergic asthma mice, offering a promising translatable strategy for the prevention and treatment of chronic allergic asthma.
This research focused on how upregulation of S100A9 contributed to the pathogenesis of the dry eye disease (DED) and whether S100A9 served as a promising therapeutic target in DED. Public single-cell RNA sequencing (scRNA-seq) data of a lacrimal gland excision (LGE) murine DED model was analyzed. LGE model was established and expression of protein was measured through immunofluorescence and western blot. DED-related signs were evaluated through tear secretion and fluorescent staining. TUNEL was performed to detect the level of cell death. Briefly, S100A9 was recognized as a highly variable gene in the DED group. LGE model was successfully established, and S100A9 showed a time-dependent increase in the corneal epithelia. Autophagic blockage was predicted by the scRNA-seq data in DED, and further verified by decrease of LC3B-II/LC3B-I and increase of SQSTM1 and p-mTOR/mTOR, while S100A9 inhibitor paquinimod (PAQ) reversed the changes. PAQ also downregulated TLR4, and inhibition of TLR4 also alleviated autophagic blockage in DED. Finally, signs of DED, chronic corneal inflammation and cell death got a remission after either inhibition of S100A9 or TLR4. In general, we deduced a S100A9-TLR4-Autophagic blockage pathway in the pathogenesis of DED.
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