Abstract：Objective To explore the association between serum nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), NIMA-related kinase 7 (NEK7) and pulmonary fibrosis among patients with coal workers' pneumoconiosis, so as to provide a basis for the assessment of the degree of pulmonary fibrosis. Methods Coal workers with pneumoconiosis hospitalized in the Second Affiliated Hospital of Xuzhou Medical University from July 2022 to July 2023 were selected by simple random sampling. Data such as age, stage of pneumoconiosis, and dust-exposure duration were collected through the hospital's electronic medical record management system. Venous blood was collected to detect the levels of serum NLRP3 and NEK7. High-resolution computed tomography (HRCT) image data of the chest were obtained through the hospital's imaging reporting system. The left and right lungs were divided into 6 pulmonary regions according to the upper, middle, and lower parts. The pulmonary fibrosis score was quantified according to the proportion of the pulmonary area occupied by HRCT manifestations of pulmonary fibrosis, including reticular shadows, pleural and interlobular septal thickening, traction bronchiectasis, and honeycombing. The association between the levels of serum NLRP3, NEK7, and pulmonary fibrosis was analyzed using a multiple linear regression model. Results A total of 81 patients with coal workers' pneumoconiosis were included, all of whom were male, with a mean age of (71.46±11.69) years. There were 48, 28, and 5 cases in stage Ⅰ, stage Ⅱ, and stage Ⅲ of pneumoconiosis pathological staging, accounting for 59.26%, 34.57%, and 6.17%, respectively. There were 45 cases of tunneling and coal mining, accounting for 55.56%. There were 41 cases with dust exposure years of ≥30 years, accounting for 50.62%. The median serum NLRP3 and NEK7 in patients with coal workers' pneumoconiosis were 2.01 (interquartile range, 2.33) ng/mL and 0.98 (interquartile range, 0.83) ng/mL. The median score of pulmonary fibrosis was 5.00 (interquartile range, 5.50) points. After adjusting for age, stage of pneumoconiosis, type of work and dust-exposure duration, multiple linear regression analysis showed that serum NLRP3 (β'=0.649) and NEK7 (β'=0.346) were positively correlated with the pulmonary fibrosis score. Conclusion The increase in the levels of serum NLRP3 and NEK7 in patients with coal workers' pneumoconiosis is related to the increase in the degree of pulmonary fibrosis.
[1] 国家卫生健康委员会规划发展与信息化司.2023年我国卫生健康事业发展统计公报[J].中国病毒病杂志,2024,14(5):416-424. Department of Planning,Development,and Information Technology,National Health Commission of the People's Republic of China.Statistical bulletin on the development of health care in China in 2023[J].Chin J Viral Dis,2024,14(5):416-424.(in Chinese) [2] 娄贺仁,王欣.我国尘肺病疾病负担的研究进展[J].中华劳动卫生职业病杂志,2023,41(2):155-160. LOU H R,WANG X.Research progress on the disease burden of pneumoconiosis in China[J].Chin J Ind Hyg Occup Dis,2023,41(2):155-160.(in Chinese) [3] HANG W L,BU C L,CUI Y M,et al.Research progress on the pathogenesis and prediction of pneumoconiosis among coal miners[J/OL].Environ Geochem Health,2024,46(9)[2025-07-01].https://doi.org/10.1007/s10653-024-02114-z. [4] QI X M,LUO Y,SONG M Y,et al.Pneumoconiosis:current status and future prospects[J].Chin Med J (Engl),2021,134(8):898-907. [5] HOY R F,DIMITRIADIS C,ABRAMSON M,et al.Prevalence and risk factors for silicosis among a large cohort of stone benchtop industry workers[J].Occup Environ Med,2023,80(8):439-446. [6] XU Y,YANG Y L,CHEN X,et al.NLRP3 inflammasome in cognitive impairment and pharmacological properties of its inhibitors[J/OL].Transl Neurodegener,2023,12(1)[2025-07-01].https://doi.org/10.1186/s40035-023-00381-x. [7] NIU T T,DE ROSNY C,CHAUTARD S,et al.NLRP3 phosphorylation in its LRR domain critically regulates inflammasome assembly[J/OL].Nat Commun,2021,12(1)[2025-07-01].https://doi.org/10.1038/s41467-021-26142-w. [8] ZHAO N,LI C C,DI B,et al.Recent advances in the NEK7-licensed NLRP3 inflammasome activation:mechanisms,role in diseases and related inhibitors[J/OL].J Autoimmun,2020,113[2025-07-01].https://doi.org/10.1016/j.jaut.2020.102515. [9] 杭文璐,武琦,李婉君,等.SiO2对大鼠气道表面微环境和NEK7/NLRP3炎性小体的影响研究[J].预防医学,2023,35(2):180-184. HANG W L,WU Q,LI W J,et al.Effect of silicon dioxide exposure on airway surface microenvironment and NEK7/NLPR3 inflammasome in rats[J].China Prev Med J,2023,35(2):180-184.(in Chinese) [10] 中华人民共和国国家卫生和计划生育委员会.职业性尘肺病的诊断:GBZ 70—2015[S].北京:中国标准出版社,2016. National Health and Family Planning Commission of the People's Republic of China.Diagnosis of occupational pneumoconiosis:GBZ 70—2015[S].Beijing:Standards Press of China,2016.(in Chinese) [11] 金盛辉,柳澄,王焕强.尘肺病胸部CT规范化检查技术专家共识(2020年版)[J].环境与职业医学,2020,37(10):943-949. JIN S H,LIU C,WANG H Q.Consensus of experts on the technical specification of chest CT examination of pneumoconiosis(2020 edition)[J].J Environ Occup Med,2020,37(10):943-949.(in Chinese) [12] 中国卫生监督协会.胸部CT辅助诊断尘肺病技术指南:T/WSJD 32—2023[S/OL].[2025-07-01].https://niohp.chinacdc.cn/sndt/202303/t20230330_264741.htm. [13] LARICI A R,BIEDERER J,CICCHETTI G,et al.ESR Essentials:imaging in fibrotic lung diseases-practice recommendations by the European Society of Thoracic Imaging[J].Eur Radiol,2025,35(4):2245-2255. [14] BANKIER A A,MACMAHON H,COLBY T,et al.Fleischner Society:glossary of terms for thoracic imaging[J/OL].Radiology,2024,310(2)[2025-07-01].https://doi.org/10.1148/radiol.232558. [15] FUJIMOTO K,TANIGUCHI H,JOHKOH T,et al.Acute exacerbation of idiopathic pulmonary fibrosis:high-resolution CT scores predict mortality[J].Eur Radiol,2012,22(1):83-92. [16] LIU T,LIU S.The impacts of coal dust on miners' health:a review[J/OL].Environ Res,2020[2025-07-01].https://doi.org/10.1016/j.envres.2020.109849. [17] SONG X,SHEN H,ZHOU L,et al.Survival analysis of 15 402 pneumoconiosis cases in Jiangsu Province of China from 1961 to 2019[J].Ann Palliat Med,2022,11(7):2291-2301. [18] 王茹,卢丽媛,李萌,等.let-7c参与肺泡巨噬细胞M2极化在煤矿粉尘致大鼠肺组织上皮-间质转化中的作用[J].环境与职业医学,2024,41(6):687-693. WANG R,LU L Y,LI M,et al.Involvement of let-7c in alveolar macrophage M2 polarization in coal mine dust-induced epithelial-mesenchymal transition in rat lung tissue[J].J Environ Occup Med,2024,41(6):687-693.(in Chinese) [19] YANG J L,WU S,HU W F,et al.Bmi1 signaling maintains the plasticity of airway epithelial progenitors in response to persistent silica exposures[J/OL].Toxicology,2022,470[2025-07-01].https://doi.org/10.1016/j.tox.2022.153152. [20] ZHOU H,ZHANG Q,LIU C Y,et al.NLRP3 inflammasome mediates abnormal epithelial regeneration and distal lung remodeling in silica-induced lung fibrosis[J/OL].Int J Mol Med,2024,53(3)[2025-07-01].https://doi.org/10.3892/ijmm.2024.5349. [21] PTASINSKI V A,STEGMAYR J,BELVISI M G,et al.Targeting alveolar repair in idiopathic pulmonary fibrosis[J].Am J Respir Cell Mol Biol,2021,65(4):347-365. [22] CHENG D M,LIAN W X,WANG T,et al.The interplay of Cxcl10+/Mmp14+ monocytes and Ccl3+ neutrophils proactively mediates silica-induced pulmonary fibrosis[J/OL].J Hazard Mater,2024,467[2025-07-01].https://doi.org/10.1016/j.jhazmat.2024.133713. [23] LIU X Y,WANG J,DOU P Y,et al.The ameliorative effects of arctiin and arctigenin on the oxidative injury of lung induced by silica via TLR-4/NLRP3/TGF-β signaling pathway[J/OL].Oxid Med Cell Longev,2021[205-07-01].https://doi.org/10.1155/2021/5598980.
