da Conceição Mendonça Jéssica, Sobral Pena João Matheus, Dos Santos Macêdo Noemi, de Souza Rodrigues Dayane, de Oliveira Dayane Alvarinho, Spencer Brady L, Lopes-Torres Eduardo José, Burcham Lindsey R, Doran Kelly S, Nagao Prescilla Emy
Laboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, Brazil.
Department of Microbiology, University of Tennessee Knoxville, Knoxville, TN 37916, USA.
Pathogens. 2023 Apr 11;12(4):580. doi: 10.3390/pathogens12040580.
(Group B , GBS) is the leading cause of neonatal sepsis and meningitis but has been recently isolated from non-pregnant adults with underlying medical conditions like diabetes. Despite diabetes being a key risk factor for invasive disease, the pathological consequences during GBS infection remain poorly characterized. Here, we demonstrate the pathogenicity of the GBS90356-ST17 and COH1-ST17 strains in streptozotocin-induced diabetic mice. We show that GBS can spread through the bloodstream and colonize several tissues, presenting a higher bacterial count in diabetic-infected mice when compared to non-diabetic-infected mice. Histological sections of the lungs showed inflammatory cell infiltration, collapsed septa, and red blood cell extravasation in the diabetic-infected group. A significant increase in collagen deposition and elastic fibers were also observed in the lungs. Moreover, the diabetic group presented red blood cells that adhered to the valve wall and disorganized cardiac muscle fibers. An increased expression of KC protein, IL-1β, genes encoding immune cell markers, and ROS (reactive oxygen species) production was observed in diabetic-infected mice, suggesting GBS promotes high levels of inflammation when compared to non-diabetic animals. Our data indicate that efforts to reverse the epidemic of diabetes could considerably reduce the incidence of invasive infection, morbidity and mortality due to GBS.
B组链球菌（GBS）是新生儿败血症和脑膜炎的主要病因，但最近已从患有糖尿病等基础疾病的非妊娠成年人中分离出来。尽管糖尿病是侵袭性疾病的关键危险因素，但GBS感染期间的病理后果仍未得到充分描述。在此，我们证明了GBS90356-ST17和COH1-ST17菌株在链脲佐菌素诱导的糖尿病小鼠中的致病性。我们发现GBS可通过血流扩散并在多个组织中定植，与未感染糖尿病的小鼠相比，感染糖尿病的小鼠体内细菌数量更高。肺部组织切片显示，糖尿病感染组有炎性细胞浸润、肺泡间隔塌陷和红细胞外渗。肺部还观察到胶原沉积和弹性纤维显著增加。此外，糖尿病组出现红细胞粘附于瓣膜壁和心肌纤维紊乱。在感染糖尿病的小鼠中观察到KC蛋白、IL-1β、编码免疫细胞标志物的基因以及活性氧（ROS）产生的表达增加，这表明与未感染糖尿病的动物相比，GBS会引发更高水平的炎症。我们的数据表明，努力扭转糖尿病流行趋势可大幅降低GBS所致侵袭性感染、发病率和死亡率。
