Baicalin Attenuates Type 2 Immune Responses in a Mouse Allergic Asthma Model through Inhibiting the Production of Thymic Stromal Lymphopoietin.

INTRODUCTION: Baicalin is a flavonoid chemical extracted and purified from the traditional Chinese medicine named Scutellaria baicalensis Georgi, which possesses broad pharmacological properties. Our work aimed to explore the protective role of baicalin in allergic asthma and its potential mechanisms on regulating type 2 immune response. METHODS: Mice were injected intraperitoneally with ovalbumin (OVA) twice, further challenged with OVA aerosol for continuous 5 days. For baicalin group, mice were pre-administrated with baicalin. After the final challenge, the immune cells in bronchoalveolar lavage fluid (BALF) and blood were examined. The cytokines were evaluated by ELISA. Histological inspections were examined by hematoxylin and eosin staining and Periodic Acid-Schiff staining. Thymic stromal lymphopoietin (TSLP) expression in lungs were detected using immunohistochemistry and Western blotting. RESULTS: The eosinophils infiltrating in BALF were reduced remarkably in baicalin-treated asthmatic mice. Baicalin decreased OVA-induced inflammatory cytokines and total serum immunoglobulin E secretion significantly. Moreover, baicalin alleviated the asthmatic pathological changes and substantially suppressed TSLP expression in the lung tissues. CONCLUSION: Our study indicates that baicalin attenuates OVA-induced allergic asthma in mice effectively by suppressing type 2 immune responses, which might provide a novel insight into the anti-asthmatic activity of baicalin.

Superparamagnetic iron oxide nanoparticles attenuate lipopolysaccharide-induced inflammatory responses through modulation of toll-like receptor 4 expression.

Superparamagnetic iron oxide nanoparticles (SPIONs) are extensively applied in biomedical fields, such as magnetic resonance imaging and as nanocarriers. However, the biosafety of SPIONs is not completely established, especially their effect on the immune system and inflammatory responses. Toll-like receptor (TLR) signaling is essential for many acute and chronic human inflammatory diseases. Regulation of TLR responses with drugs is helpful for these inflammatory conditions. In this study, we investigated the effects of 10 and 30 nm SPIONs on macrophages in the presence or absence of the TLR4 agonist lipopolysaccharide (LPS). We found that SPIONs inhibited the release of inflammatory cytokines induced by LPS both in murine and human macrophages in a concentration-dependent manner. Meanwhile, SPIONs suppressed inducible nitric oxide synthase expression activated by SPIONs in RAW264.7 macrophages. Additionally, TLR4 mRNA transcription and expression were attenuated with SPIONs treatment, which positively correlated with the release of inflammatory cytokines. In summary, our study demonstrates that SPIONs can suppress inflammatory responses, and the underlying mechanism may be regulated by TLR4 expression. Our present work contributes to clarifying the biosafety of SPIONs and provides a potential approach to alleviate human inflammatory diseases.

Iron oxide nanoparticles size-dependently activate mouse primary macrophages via oxidative stress and endoplasmic reticulum stress.

Iron oxide nanoparticles (IONPs) are widely used in cosmetics, food additives, and biomedical fields. There are a few adverse effects of IONPs according to clinical reports and animal studies. However, the immunotoxicity and, in particular, the size effects and mechanisms of IONPs on macrophages have not been fully clarified. This study aimed to explore the impacts of 10 nm and 30 nm IONPs on immune responses both in mice and bone marrow-derived macrophages (BMMs). We found that 10 mg/kg IONPs elevated the number of neutrophils and the level of interleukin-6 (IL-6) in peritoneal lavage fluids in mice. IONPs also provoked BMMs and induced the production of IL-6 and tumor necrosis factor-α (TNF-α). The impacts of IONPs on inflammatory responses were size-dependent, and 30 nm IONPs were stronger. Consistently, RNA-sequencing and bioinformatic analysis showed that 30 nm IONPs activated numerous biological processes, including many immune responses, endoplasmic reticulum (ER) stress, and oxidative stress. Furthermore, the inflammatory response caused by IONPs could be attenuated by blocking actin polymerization, ER stress, or oxidative stress. This study is helpful to understand the biosafety of IONPs and protect humans from their potential adverse immune effects.