Argentina Fifa, Suwarsa Oki, Gunawan Hendra, Berbudi Afiat
Doctoral Program in Medical Science, Faculty of Medicine, Universitas Padjadjaran, Bandung, West Java, Indonesia.
Department of Dermatology and Venereology, Faculty of Medicine, Universitas Sriwijaya/Mohammad Hoesin General Hospital, Palembang, South Sumatera, Indonesia.
Clin Cosmet Investig Dermatol. 2023 Jun 12;16:1485-1492. doi: 10.2147/CCID.S405932. eCollection 2023.
Leprosy, a chronic infectious peripheral neuropathy, is caused by . This bacterium produces triacylated lipopeptides that can induce the immune system via the Toll-like receptor 2/1 (TLR 2/1) complex. Activation of TLR 2/1 produces proinflammatory cytokines and antimicrobial peptides (AMPs), including human beta-defensin-3 (HBD-3) and cathelicidin.
To analyze differences in gene expression of HBD-3 and cathelicidin in the skin of leprosy patients, household contacts, and healthy individuals.
An analytic observational study was conducted at the Outpatient Clinic of Dermatology and Venereology of Dr Mohammad Hoesin General Hospital, Palembang, Indonesia, from January 2021 to June 2022. In each group of 18 subjects, 72 samples were collected, including skin lesion in leprosy patients, normal skin in leprosy patients, household contacts, and healthy individuals. A comparison of HBD-3 and cathelicidin gene expression between the four groups was analyzed using Pearson Chi Square, Kruskal-Wallis, and Mann-Whitney Test.
The median value of HBD-3 gene expression on skin lesion in leprosy patients was 260.61 (0.19-3734.10); normal skin in leprosy patients was 1.91 (0.01-151.17); household contacts skin was 7.93 (0.27-121.10); and healthy individuals' skin was 1.00 (1.00-1.00) is highly significant difference ( < 0.0001). The median value of cathelicidin gene expression on skin lesion in leprosy patients was 38.72 (0.28-1852.17); normal skin in leprosy patients was 0.48 (0.01-15.83); household contacts skin was 9.8 (0.04-128.0); and healthy individual skin was 1.00 (1.00-1.00), also highly significant difference (p < 0.0001).
Gene expression of HBD-3 and cathelicidin increased in skin lesions of leprosy patients and household contacts.
麻风病是一种慢性感染性周围神经病变，由……引起。这种细菌产生三酰化脂肽，可通过Toll样受体2/1（TLR 2/1）复合物诱导免疫系统。TLR 2/1的激活产生促炎细胞因子和抗菌肽（AMPs），包括人β-防御素-3（HBD-3）和杀菌肽。
分析麻风病患者、家庭接触者和健康个体皮肤中HBD-3和杀菌肽基因表达的差异。
2021年1月至2022年6月在印度尼西亚巨港穆罕默德·霍辛综合医院皮肤科和性病门诊进行了一项分析性观察研究。在每组18名受试者中，共收集72个样本，包括麻风病患者的皮肤病变、麻风病患者的正常皮肤、家庭接触者以及健康个体的皮肤。使用Pearson卡方检验、Kruskal-Wallis检验和Mann-Whitney检验分析四组之间HBD-3和杀菌肽基因表达的差异。
麻风病患者皮肤病变中HBD-3基因表达的中位数为260.61（0.19 - 3734.10）；麻风病患者正常皮肤中为1.91（0.01 - 151.17）；家庭接触者皮肤中为7.93（0.27 - 121.10）；健康个体皮肤中为1.00（1.00 - 1.00），差异具有高度显著性（<0.0001）。麻风病患者皮肤病变中杀菌肽基因表达的中位数为38.72（0.28 - 1852.17）；麻风病患者正常皮肤中为0.48（0.01 - 15.83）；家庭接触者皮肤中为9.8（0.04 - 128.0）；健康个体皮肤中为1.00（1.00 - 1.00），差异也具有高度显著性（p<0.0001）。
麻风病患者和家庭接触者的皮肤病变中HBD-3和杀菌肽的基因表达增加。
