Jiang Nan, Zhong Yong-Cong, Lin Qing-Rong, Song Chen-Sheng, Yu Bin, Hu Yan-Jun
Division of Orthopaedics and Traumatology, Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Guangdong Provincial Key Laboratory of Bone and Cartilage Regenerative Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Int J Immunogenet. 2023 Jun;50(3):127-133. doi: 10.1111/iji.12620. Epub 2023 Apr 25.
Genetic variations in the solute carrier family 11 member 1 (SLC11A1) gene have been implicated in developing inflammatory disorders. However, it is still unclear whether such polymorphisms contribute to the pathogenesis of post-traumatic osteomyelitis (PTOM). Therefore, this study investigated the roles of genetic variations of the SLC11A1 gene (rs17235409 and rs3731865) in PTOM development in a Chinese Han cohort. The SNaPshot method was used for genotyping 704 participants (336 patients and 368 controls) for rs17235409 and rs3731865. Outcomes revealed that rs17235409 increased the risk of PTOM occurrence by dominant (p = .037, odds ratio [OR] = 1.44) and heterozygous models (p = .035, OR = 1.45), implying AG genotype as a risk factor for PTOM development. In addition, patients with AG genotype had relatively higher levels of inflammatory biomarkers than those with AA and GG genotypes, especially for the white blood cell count and C-reactive protein. Despite no statistically significant differences achieved, rs3731865 may reduce the PTOM susceptibility, suggested by the results of dominant (p = .051, OR = 0.67) and heterozygous (p = .068, OR = 0.69) models. In short, rs17235409 confers an elevated chance of developing PTOM, with AG genotype as a risk factor. Whether rs3731865 involves in the pathogenesis of PTOM requires further investigations.
溶质载体家族11成员1(SLC11A1)基因的遗传变异与炎症性疾病的发生有关。然而,这些多态性是否促成创伤后骨髓炎(PTOM)的发病机制仍不清楚。因此,本研究调查了SLC11A1基因(rs17235409和rs3731865)的遗传变异在中国汉族队列PTOM发生中的作用。采用SNaPshot方法对704名参与者(336例患者和368例对照)进行rs17235409和rs3731865基因分型。结果显示,rs17235409通过显性模型(p = 0.037,优势比[OR]=1.44)和杂合模型(p = 0.035,OR = 1.45)增加了PTOM发生的风险,提示AG基因型是PTOM发生的危险因素。此外,AG基因型患者的炎症生物标志物水平相对高于AA和GG基因型患者,尤其是白细胞计数和C反应蛋白。尽管未达到统计学显著差异,但显性模型(p = 0.051,OR = 0.67)和杂合模型(p = 0.068,OR = 0.69)的结果表明,rs3731865可能降低PTOM易感性。简而言之,rs17235409增加了发生PTOM的几率,AG基因型是危险因素。rs3731865是否参与PTOM的发病机制需要进一步研究。