Background The highly polymorphic intedeukin 10.G （IL10.G） microsatellite located in the promoter region of the interleukin-10 （IL-10） gene exerts a positive transcriptional regulatory effect on IL-10 gene expression and correlates with the in vitro IL-10 secretion. This study was conducted to investigate whether IL10.G microsatellite is associated with the incidence and/or the outcome of severe sepsis. Methods One hundred and fifteen patients with severe sepsis who had been treated at the intensive care unit of the university hospital were studied. One hundred and forty-one healthy individuals served as controls. IL10.G microsatellite genotyping was performed with the following two methods： fluorescent based polymerase chain reaction （PCR） techniques and silver staining of the amplified DNA fragment in polyacrylamide gel. Alleles were defined according to the size of the amplified DNA product. Results Ten alleles and 36 genotypes were detected both in the patients with severe sepsis and in the healthy controls. Allele IL10.G9 and allele IL10.G13 were the commonest alleles with the frequencies of 32.6% and 21.3% respectively in the patients with severe sepsis, and 34% and 27% respectively in the healthy controls. The allele frequencies of IL10.G microsatellite were neither different between the patients with severe sepsis and the healthy controls （P 〉 0.05）, nor between survivors and non-survivors （P 〉 0.05）. However, the frequency of one common allele IL10.G13 was slightly lower in the patients with severe sepsis than in the healthy controls （21.3% vs 27%, P 〉 0.05）, and the frequency of allele IL10.G9 was slightly higher in the non-survivors than in the survivors （37.1% vs 28.1%, P 〉 0.05）.Conclusion IL10.G microsatellite may neither contribute to the susceptibility to severe sepsis nor to the fatal outcome of severe sepsis.
SHU QiangSHI Chang-chunZHANG Xiang-hongSHI ZhuoSHI Shan-shanFANG Xiang-mingCHEN Qi-xingStuber Frank
严重损伤后全身性炎症反应失控及器官损害受体内众多基因的调控，为何有的人群容易并发脓毒症（sepsis）和多器官功能障碍综合征（muhipe organ dysfunction syndrome，MODS）等感染并发症？同样，对严重感染患者虽然采取相似的治疗方案，但个体的反应和预后可能完全不同。这些现象是否与体内存在某种脓毒症和MODS相关的特异性基因或基因表达特性的改变影响宿主对应激状态的敏感有关？这一问题正日益引起人们的兴趣与关注。近年来，随着人类基因组学研究的不断深入，医学工作者逐渐认识到遗传学机制的差异性是许多疾病发生、发展中内因的物质基础。脓毒症是由环境因素（病原微生物等）和遗传因素共同作用的多基因征侯群，多个常见的、微效的遗传变异独立或相互间通过目前尚未能阐明的分子机制在脓毒症的发生、发展中起着一定作用，不同个体对脓毒症的易感性和预后存在明显的差异。
