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.

Lung adenocarcinoma (LADC) is a major subtype of lung cancer, particularly among populations of East Asia. The epidermal growth factor receptor (EGFR) is the most frequently mutated oncogene promoting LADC progression and can serve as a therapeutic target in LADC. The tissue inhibitor of metalloproteinases (TIMP)-3 is a major regulator of extracellular matrix turnover via targeting of matrix metalloproteinases (MMPs), and thus, plays a critical role in tumor development and progression. The purpose of this study was to investigate potential associations among TIMP-3 genetic polymorphisms, EGFR statuses, and cancer clinicopathologic development in patients with LADC. In this study, 277 LADC patients with different EGFR statuses were recruited to dissect the allelic discrimination of TIMP-3 -1296 T>C (rs9619311), TIMP3 249T>C (rs9862), and TIMP3 261C>T (rs11547635) polymorphisms using a TaqMan allelic discrimination assay. Our data showed that compared to those LADC patients with wild-type CC homozygotes of TIMP-3 rs9862, patients harboring TT homozygotes of rs9862 were at a higher risk of developing mutant EGFR (adjusted odds ratio (AOR) = 2.530; 95% confidence interval (CI): 1.230–5.205; p = 0.012), particularly the EGFR L858R point mutation (AOR = 2.975; 95% CI: 1.182–7.488; p = 0.021). Moreover, we observed that TIMP-3 TT homozygotes of rs9862 were correlated with the incidence of EGFR mutations in patients with a smoking habit (p = 0.045). Within male patients harboring a mutant EGFR, TIMP-3 rs9862 T (CT+TT) allele carriers were at higher risk of developing an advanced stage (p = 0.025) and lymph node metastasis (p = 0.043). Further analyses of clinical datasets revealed correlations of TIMP-3 expression with a favorable prognosis in patients with LADC. In conclusion, the data suggest that TIMP-3 rs9862 polymorphisms may contribute to identify subgroups of lung cancer patients at high risk for tumor progression, among carriers of LADC-bearing mutant EGFR.

Non-small cell lung cancer (NSCLC) is a typical inflammation-associated cancer, and lung adenocarcinoma (LUAD) is the most common histopathological subtype. Epidermal growth factor receptor (EGFR) mutations are the most common driver mutations of LUAD, and they have been identified as important therapeutic targets by EGFR tyrosine kinase inhibitors. Interleukin (IL)-17A secreted by T-helper 17 lymphocytes is a proinflammatory cytokine that plays an important role in cancer pathogenesis. The present study was designed to investigate the possible associations among IL-17A genetic polymorphisms, EGFR mutation status, and the clinicopathologic development of LUAD in a Taiwanese population. Our study population consisted of 277 LUAD patients harboring the wild-type (WT) EGFR or a mutant (MT) EGFR. Four single-nucleotide polymorphisms (SNPs) of IL-17A in the peripheral blood, including rs8193036(C > T), rs8193037(G > A), rs2275913(G > A), and rs3748067(C > T) loci, were genotyped using a TaqMan allelic discrimination assay. Our results showed that none of these IL-17A SNPs were correlated with the risk of developing mutant EGFR. However, patients with a smoking habit who carried the GA genotype of IL-17A rs8193037 had a significantly lower susceptibility to EGFR mutations (adjusted odds ratio (AOR): 0.225; 95% confidence interval (CI): 0.056~0.900, p = 0.035). Moreover, compared to individuals carrying the CC genotype of rs8193036 at IL-17A, T-allele carriers (CT + TT) were at higher risk of developing more-advanced stages (stage III or IV; p = 0.020). In the WT EGFR subgroup analysis, IL-17A rs8193036 T-allele carriers had higher risks of developing an advanced tumor stage (p = 0.016) and lymphatic invasion (p = 0.049). Further analyses of clinical datasets revealed correlations of IL-17 receptor A (IL-17RA) and IL-17RC expressions with a poor prognosis of LUAD patients with a smoking history or with higher levels of tumor-infiltrating lymphocytes. In conclusion, our results suggested that two functional promoter polymorphisms of IL-17A, i.e., rs8193036 and rs8193037, were associated with the EGFR mutation status and progression in LUAD patients, indicating that these two genetic variants might act as possible markers for predicting patients’ clinical prognoses.

Industrial zones are prevalent in central Taiwan, with major sources of ambient air pollution including large thermal power plants and steel manufacturing facilities. Fine particulate matter (PM₂.₅) is a critical component of air pollution and has been implicated in the development and progression of chronic respiratory diseases (CRDs), primarily through pathways involving immune dysregulation and persistent low-grade inflammation. Oligo-fucoidan (OF), a low–molecular-weight derivative of fucoidan, has been reported to exert immunomodulatory and anti-inflammatory effects in experimental and preclinical studies. However, clinical evidence regarding its potential role in air pollution–associated respiratory conditions remains limited. This exploratory, non-randomized, open-label study aimed to descriptively evaluate changes in immune and inflammatory parameters among patients with air pollution–associated chronic pulmonary diseases residing in central Taiwan. A total of 46 participants received OF supplementation (2.2 g daily) for 12 weeks in addition to standard care. Blood samples were collected at baseline and at weeks 4, 8, and 12 to assess biochemical indices, lymphocyte subsets, inflammatory cytokines, and serum heavy metal concentrations. Ambient PM₂.₅ data during the study period were obtained from nearby governmental air quality monitoring stations. Ambient PM₂.₅ concentrations during the study period were within a relatively low range (11.1 ± 4.0 to 14.7 ± 10.3 µg/m³). Over the 12-week supplementation period, descriptive variations were observed in several immune and inflammatory markers, including white blood cell count, C-reactive protein, ferritin levels, lymphocyte subset distributions, and selected cytokines. Serum mercury concentrations demonstrated a positive association with ambient PM₂.₅ levels. Among the measured cytokines, IL-8 values at later time points were lower than at baseline; these changes are presented descriptively and should be interpreted cautiously given the exploratory, single-arm nature of the study. This exploratory study provides a descriptive characterization of immune, inflammatory, and heavy metal–related parameters in patients with air pollution–associated chronic pulmonary diseases receiving oligo-fucoidan as an adjunct to standard therapy. While causal relationships and statistically confirmed longitudinal effects cannot be established, these preliminary observations may inform the design of future controlled trials and mechanistic investigations in the context of environmental respiratory health.