RESUMO
OBJECTIVE: To explore the association of serum Apelin level, silicosis stage and lung function in patients with occupational silicosis(hereinafter referred to as silicosis). METHODS: A case-control study was conducted. A total of 85 patients with silicosis were selected as the silicosis group(44, 28 and 13 patients with stage Ⅰ, Ⅱ and Ⅲ silicosis, respectively), and 120 healthy individuals without occupational hazard exposure were selected as the control group. Serum samples were collected from the cases of the two groups and the level of Apelin was determined by enzyme-linked immunosorbent assay. The pulmonary function of the silicosis group was examined. RESULTS: The median and the 25 th and 75 th percentiles \[M(P_(25),P_(75))\] of serum Apelin levels in the control group and silicosis group were 1.29(0.92, 1.77) and 0.80(0.62, 1.04) mg/L, respectively. The level of serum Apelin M(P_(25),P_(75)) in stage Ⅰ, Ⅱ and Ⅲ silicosis patients was 1.03(0.82, 1.31), 0.66(0.60, 0.80) and 0.50(0.30, 0.65) mg/L, respectively. The results of multiple linear regression analysis showed that the level of serum Apelin in the silicosis group was higher than that in the control group after excluding the influence of age and smoking(P<0.01). The level of serum Apelin decreased with the increase of silicosis stage in the silicosis group(P<0.001). Serum Apelin level in silicosis group was positively correlated with lung vital capacity, forced vital capacity, forced expiratory volume in the first second, and forced expiratory flow between 25% and 75%(all P<0.05). CONCLUSION: The lower level of serum Apein in silicosis patients, the more serious the disease and the more serious the damage to lung function. Apelin is of significance in the diagnosis, staging, treatment appraisal and prognostic evaluation of silicosis, and it can be use as a potential therapeutic target for silicosis.
RESUMO
Silica dust is one of the main occupational hazards in various industries. In addition to causing occupational silicosis, silica dust can also stimulate innate and acquired immunity and induce autoimmune diseases(AID) such as systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, and antineutrophil cytoplasmic antibody(ANCA)-associated vasculitis. Silica dust exposure can induce changes in the levels of autoantibodies in vivo, such as rheumatoid factor, antinuclear antibody, ANCA, anti-centromere antibody, anti-topoisomerase Ⅰ antibody, anti-desmoglein antibody, anti-centromere antigens-B antibody, anti-carbamylated protein antibody, anti-smooth muscle antibody and anti-glomerular basement membrane antibody. At present, the mechanism of autoimmune disorders induced by silica dust has not yet been fully elucidated. The current research suggests that it is related to cell apoptosis of alveolar macrophages, the disorder of the Fas/Fas ligand system, the imbalance of T cell proportion, and the dysregulation of T helper cell(Th) 1 and Th2 type cytokines homeostasis. Understanding the pathogenesis of autoimmune disorders induced by silica dust and exploring possible therapeutic targets will provide new ideas for the treatment of silicosis.
