Tang Ling, Wang Hui, Cao Kangli, Li Yajuan, Li Tingting, Huang Ying, Xu Yuanhong
Department of Clinical Laboratory, First Affiliated Hospital of Anhui Medical University, Hefei, People's Republic of China.
Infect Drug Resist. 2023 Feb 28;16:1221-1230. doi: 10.2147/IDR.S391349. eCollection 2023.
() is a Gram-negative bacterium that is predominantly associated with liver abscesses in global diabetic patients. High levels of glucose in the surrounding of increase its pathogenicity including capsular polysaccharide (CPS) and fimbriae. Other important virulent factors include outer membrane protein A (ompA) and regulator mucoid phenotype A (rmpA). The objective of this investigation was to elucidate the effects of high glucose on and gene expression and serum resistance of causing liver abscess.
The clinical history of 57 patients suffering from -caused liver abscesses (KLA) was acquired and their clinical and laboratory manifestations in the presence or absence of diabetes were analyzed. The antimicrobial susceptibility, serotypes, and virulence genes were tested. Clinical isolates of 3 serotype-K1 hypervirulent (hvKP) were used to detect the effect of exogenous high glucose on , and genes expression, and bacterial serum resistance.
KLA patients with diabetes showed higher C-reactive protein (CRP) compared to non-diabetic KLA patients. Furthermore, the diabetic group showed increased incidences of sepsis and invasive infections, and their length of hospital stay was also prolonged. Pre-incubation of in high glucose (0.5%) concentration up-regulated , and genes expression. However, cAMP supplementation, which was inhibited by environmental glucose, reversed the increase of and in a cAMP-dependent manner. Moreover, hvKP strains incubated in high glucose also exhibited enhanced protection from serum killing.
High glucose levels reflected by poor glycemic control has increased gene expression of and in hvKP by the cAMP signaling pathway and enhanced its resistance to serum killing, thus providing a new and reasonable explanation for the high incidences of sepsis and invasive infections in KLA patients with diabetes.
（某种细菌名称）是一种革兰氏阴性菌，在全球糖尿病患者中主要与肝脓肿相关。其周围环境中的高糖水平会增加其致病性，包括荚膜多糖（CPS）和菌毛。其他重要的毒力因子包括外膜蛋白A（ompA）和调节黏液样表型A（rmpA）。本研究的目的是阐明高糖对导致肝脓肿的（细菌名称）的（相关基因名称）基因表达和血清抗性的影响。
获取了57例由（细菌名称）引起的肝脓肿（KLA）患者的临床病史，并分析了他们在有或无糖尿病情况下的临床和实验室表现。检测了抗菌药敏性、血清型和毒力基因。使用3株血清型K1高毒力（hvKP）的临床分离株来检测外源性高糖对（相关基因名称）基因表达和细菌血清抗性的影响。
与非糖尿病KLA患者相比，糖尿病KLA患者的C反应蛋白（CRP）更高。此外，糖尿病组的败血症和侵袭性感染发生率增加，住院时间也延长。在高糖（0.5%）浓度下预孵育（细菌名称）会上调（相关基因名称）基因表达。然而，环境葡萄糖抑制的cAMP补充以cAMP依赖的方式逆转了（相关基因名称）的增加。此外，在高糖中孵育的hvKP菌株对血清杀伤的抵抗力也增强。
血糖控制不佳所反映的高糖水平通过cAMP信号通路增加了hvKP中（相关基因名称）的基因表达，并增强了其对血清杀伤的抗性，从而为糖尿病KLA患者败血症和侵袭性感染的高发生率提供了新的合理的解释。
