社区获得性肺炎(CAP)是院外发病和死亡主要原因。在大多数CAP患者发生炎症反应综合征和败血症,持续平衡抗炎因子和促炎因子之间的平衡。主要促炎因子有IL-6、TNF,败血症时也产生对抗炎症反应的因子IL-10,从而抑制促炎因子IL-6、IL-1α、IL-1β、IL-8和TNF。不同细胞因子基因水平对应激刺激的反应是不同的。本文旨在探讨诱导基因表达的IL-6和IL-10启动区单核苷酸多肽性与CAP之间的关系。 Community acquired pneumonia (CAP) is the leading cause of outpatient morbidity and mortality. Inflammatory syndrome and sepsis occur in most patients with CAP, and the balance between anti-inflammatory and proinflammatory cytokines is continually balanced. IL-6, TNF, and sepsis are also the major proinflammatory cytokines. They also produce anti-inflammatory cytokine IL-10 and thus inhibit the proinflammatory cytokines IL-6, IL-1α, IL-1β, IL-8 and TNF. The response of different cytokine gene levels to stress stimulation is different. This article aims to investigate the relationship between single nucleotide polymorphisms in the promoter region of IL-6 and IL-10 that induce gene expression and CAP.