Asthma is a common disease occurring worldwide. The clinical treatment of asthma is constantly revised and updated; however, it is associated with side effects. Our previous in vitro and ex vivo studies found that oligo-fucoidan can improve allergic immune responses and reduce airway inflammation. The purpose of this clinical trial was to investigate the effects of oligo-fucoidan on the immune status, inflammatory response, and pulmonary function of patients with asthma. Twenty asthmatic patients were randomly divided into two groups: (1) control group: receiving regular asthma treatment and supplementation with placebo; (2) fucoidan group: receiving regular asthma treatment and supplementation with oligo-fucoidan. Pulmonary function tests, the "Asthma Control Questionnaire" survey, biochemical data, inflammatory factors, and immune cell subtypes were detected. During treatment, the levels of WBC (p = 0.038) and creatinine (p = 0.012 and p = 0.008 at 12th and 24th weeks) were significantly decreased in the fucoidan group. Lung function (FEV₁/FVC pr) significantly increased in the fucoidan group (p = 0.046). Regarding the proportion of immune cells, the level of IFN⁺ and CD4⁺IFN⁺cells in the fucoidan group was significantly increased during the treatment period (P < 0.05), while the proportions of CD3⁺CD4⁺ cells (p = 0.048) and CD3⁺CD8⁺ cells (p = 0.009) in the fucoidan group were significantly decreased during the treatment period. Regarding cytokines, the level of interleukin-8 (IL-8) was also significantly reduced in the fucoidan group during the treatment period.

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.

In the pathogenesis of asthma, the proliferation of airway smooth muscle cells (ASMCs) is a key factor in airway remodeling and causes airway narrowing. In addition, ASMCs are also the effector cells of airway inflammation. Fucoidan extracted from marine brown algae polysaccharides has antiviral, antioxidant, antimicrobial, anticlotting, and anticancer properties; however, its effectiveness for asthma has not been elucidated thus far. Platelet-derived growth factor (PDGF)-treated primary ASMCs were cultured with or without oligo-fucoidan (100, 500, or 1000 µg/mL) to evaluate its effects on cell proliferation, cell cycle, apoptosis, and Akt, ERK1/2 signaling pathway. We found that PDGF (40 ng/mL) increased the proliferation of ASMCs by 2.5-fold after 48 h (p < 0.05). Oligo-fucoidan reduced the proliferation of PDGF-stimulated ASMCs by 75%–99% after 48 h (p < 0.05) and induced G₁/G₀ cell cycle arrest, but did not induce apoptosis. Further, oligo-fucoidan supplementation reduced PDGF-stimulated extracellular signal-regulated kinase (ERK1/2), Akt, and nuclear factor (NF)-κB phosphorylation. Taken together, oligo-fucoidan supplementation might reduce proliferation of PDGF-treated ASMCs through the suppression of ERK1/2 and Akt phosphorylation and NF-κB activation. The results provide basis for future animal experiments and human trials.

Chronic hepatitis B (CHB) is a common chronic disease. Previous studies have shown a link between 25-hydroxyvitamin D₃ (vitamin D₃) concentration and liver disease. Hepatitis B virus (HBV) infection has been attributed to the inappropriate functioning of cell-mediated immunity. However, the effects of vitamin D₃, immune cell, and HBeAg status on HBV viral load in CHB patients are still unclear. We investigated the relationship between the serum concentration of vitamin D₃, percentage of immune cells in peripheral blood, and the HBV viral load of CHB patients. Sixty CHB patients were recruited, and their blood samples were collected and analyzed. Vitamin D level was measured using a chemiluminescence assay. A level of 30 ng/mL or above was defined as a vitamin D₃ sufficiency. We assigned vitamin D₃ status as either normal (≥30 ng/mL), insufficient (20–30 ng/mL), or deficient (<20 ng/mL). T-lymphocyte and B-lymphocyte surface markers in peripheral blood were detected using flow cytometry. The factors associated with HBV viral load were analyzed using univariate and multivariate-adjusted models. The mean serum vitamin D₃ concentration in the subjects was 20.9 ± 5.6 ng/mL. Up to 88.3% of the patients were either deficient in or had insufficient vitamin D₃. The gender, BMI, hepatitis B surface antigen levels, and ALT levels were significantly related to serum vitamin D₃ levels. Serum vitamin D₃ concentration, HBe status, HBs levels, ALT, and AST levels showed a statistically significant correlation with the HBV DNA levels. Serum vitamin D₃ concentrations and hepatitis B surface antigen levels were strongly correlated with HBV DNA levels. Vitamin D₃ levels were significantly associated with CD19 numbers (β:−6.2, 95% CI: −10.5). In multivariate analysis, vitamin D₃ levels in the deficient and insufficient groups, and the CD8, HBeAg, and WBC counts were significantly associated with HBV DNA levels. In the immune tolerance phase of HBeAg-negative chronic HBV infection, vitamin D₃ may be a modulator of immune function via CD8, CD19, and HBV DNA.