Gupta Ena, Kumar Sanni, Srivastava Vijay Kumar, Saxena Juhi, Siddiqui Arif Jamal, Mehta Sudhir, Kaushik Sanket, Jyoti Anupam
Amity Institute of Biotechnology, Amity University Rajasthan, Amity Education Valley, Kant Kalwar, NH-11C, Jaipur-Delhi Highway, Jaipur 303002, Rajasthan, India.
Department of Biotechnology, University Institute of Biotechnology, Chandigarh University, S.A.S Nagar 140413, Punjab, India.
Vaccines (Basel). 2022 Oct 1;10(10):1648. doi: 10.3390/vaccines10101648.
Previous reports from our lab have documented dysregulated host inflammatory reactions in response to bacterial infections in sepsis. Both Gram-negative bacteria (GNB) and Gram-positive bacteria (GPB) play a significant role in the development and progression of sepsis by releasing several virulence factors. During sepsis, host cells produce a range of inflammatory responses including inducible nitric oxide synthase (iNOS) expression, nitrite generation, neutrophil extracellular traps (NETs) release, and pro-inflammatory cytokines production. The current study was conducted to discern the differences in host inflammatory reactions in response to both and along with the organ dysfunction parameters in patients of sepsis. We examined 60 ICU sepsis patients identified based on the Acute Physiology and Chronic Health Evaluation II (APACHE II) and Sequential Organ Failure Assessment (SOFA II) scores. Pathogen identification was carried out using culture-based methods and gene-specific primers by real-time polymerase chain reaction (RT-PCR). Samples of blood from healthy volunteers were spiked with (GNB) and (GPB). The incidence of NETs formation, iNOS expression, total nitrite content, and pro-inflammatory cytokine level was estimated. Prevalence of , (both GNB), , and (both GPB) was found in sepsis patients. Augmented levels of inflammatory mediators including expression, total nitrite, the incidence of NETs, and proinflammatory cytokines, during spiking, were found in response to infections in comparison with infections. These inflammatory mediators were found to be positively correlated with organ dysfunction in both GN and GP infections in sepsis patients. Augmented host inflammatory response was generated in infections as compared with .
我们实验室之前的报告记录了脓毒症中宿主对细菌感染的炎症反应失调。革兰氏阴性菌（GNB）和革兰氏阳性菌（GPB）都通过释放多种毒力因子在脓毒症的发生和发展中起重要作用。在脓毒症期间，宿主细胞会产生一系列炎症反应，包括诱导型一氧化氮合酶（iNOS）表达、亚硝酸盐生成、中性粒细胞胞外陷阱（NETs）释放以及促炎细胞因子产生。本研究旨在识别脓毒症患者中宿主对GNB和GPB的炎症反应差异以及器官功能障碍参数。我们检查了60例根据急性生理与慢性健康状况评估II（APACHE II）和序贯器官衰竭评估（SOFA II）评分确定的重症监护病房脓毒症患者。使用基于培养的方法和实时聚合酶链反应（RT-PCR）的基因特异性引物进行病原体鉴定。将来自健康志愿者的血液样本分别加入大肠埃希菌（GNB）和金黄色葡萄球菌（GPB）。估计NETs形成、iNOS表达、总亚硝酸盐含量和促炎细胞因子水平的发生率。在脓毒症患者中发现了大肠埃希菌、肺炎克雷伯菌（均为GNB）、金黄色葡萄球菌和表皮葡萄球菌（均为GPB）的感染。与GPB感染相比，在加入大肠埃希菌感染后，发现炎症介质水平升高，包括iNOS表达、总亚硝酸盐、NETs发生率和促炎细胞因子。在脓毒症患者的GN和GP感染中，这些炎症介质均与器官功能障碍呈正相关。与GPB感染相比，大肠埃希菌感染产生了增强的宿主炎症反应。
