An imbalance in the helper T cells (Th)1/Th2 and regulatory T cells (Tregs)/Th17 ratios is believed to play a key role in asthmatic inflammatory responses. Fucoidan reportedly reduces the production of inflammatory factors. Nutritional intervention is an important tool in decreasing the severity of asthmatic disease. This study aimed to investigate the beneficial roles of oligo-fucoidan in balancing the T cell subtype ratios and reducing airway inflammation ex vivo. Peripheral blood mononuclear cells (PBMCs) were collected from 30 asthmatic subjects and 15 healthy subjects. Harvested PBMCs were stimulated and treated with or without oligo-fucoidan (100 or 500 µg/ml) for 48 h. Cell surface and intracellular cytokine markers were examined by flow cytometry. The pro-inflammatory factors in plasma and culture supernatants were measured using ELISA kits. We found that oligo-fucoidan increases the proportion of Th1 and Treg cells, but did not affect the proportion of Th2 and Th17 cells. Oligo-fucoidan also increased the levels of interferon-γ and interleukin-10. Thus, we concluded that oligo-fucoidan might improve the imbalance in Th1/Th2 and Treg/Th17 ratios to reduce airway inflammation, which could be a potential adjuvant therapy for allergic asthma.
Inflammation of airway smooth muscle cells (ASMCs) is believed to be important in causing airway hyperresponsiveness. However, zinc has been reported to be implicated in many kinds of cell inflammation. Little is known about the effect of zinc treatment on Der p2 (group II Dermatophagoides pteronyssinus)-induced inflammation from ASMCs. This study investigated effects and mechanisms of zinc in Der p2-treated ASMCs. Der p2-treated primary ASMCs were cultured with various concentrations of zinc sulfate (ZnSO₄) 6 μM, 12 μM, 24 μM, and 96 μM. The proteins and mRNAs of cytokines in ASMCs were examined by ELISA and real-time PCR. Intracellular zinc was stained with Zinquin fluorescence. The cell signaling protein expression was detected by Western blot. Der p2 was used to induce interleukin (IL)-6, IL-8, IL-1, and monocyte chemotactic protein-1 production of ASMCs. However, we found that 24 μM ZnSO₄ reduced these inflammatory mediators production of Der p2-treated primary ASMCs. Der p2-induced extracellular signal-regulated kinases (ERK) and nuclear factor-kappa B (NF-κB) phosphorylation were suppressed by supplementation of 24 μM ZnSO₄. Zinc is an anti-inflammatory agent that reduces inflammation of Der p2-treated ASMCs through the suppression of the ERK and NF-κB pathway. The results may be helpful for the development of effective treatments.
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