早期细胞募集缺陷导致糖尿病小鼠对呼吸道肺炎克雷伯菌感染的易感性增加。
Defects in early cell recruitment contribute to the increased susceptibility to respiratory Klebsiella pneumoniae infection in diabetic mice.
作者信息
Martinez Nuria, Ketheesan Natkunam, Martens Gregory W, West Kim, Lien Egil, Kornfeld Hardy
机构信息
Division of Pulmonary, Allergy and Critical Care, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA.
Division of Pulmonary, Allergy and Critical Care, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA; Australian Institute of Tropical Health and Medicine, James Cook University, Queensland 4811, Australia.
出版信息
Microbes Infect. 2016 Oct;18(10):649-655. doi: 10.1016/j.micinf.2016.05.007. Epub 2016 May 30.
Diabetes is associated with increased susceptibility to Klebsiella pneumoniae and poor prognosis with infection. We demonstrate accelerated mortality in mice with streptozotocin-induced diabetes following tracheal instillation of K. pneumoniae. Diabetic mice recruited fewer granulocytes to the alveolar airspace and had reduced early production of CXCL1, CXCL2, IL-1β and TNF-α following tracheal instillation of K. pneumoniae-lipopolysaccharide. Additionally, TLR2 and TIRAP expression following K. pneumoniae-lipopolysaccharide exposure was decreased in hyperglycemic mice. These findings indicate that impaired innate sensing and failure to rapidly recruit granulocytes to the site of infection is a mechanism for diabetic susceptibility to respiratory K. pneumoniae infection.
糖尿病与肺炎克雷伯菌易感性增加及感染预后不良相关。我们证明，在气管内注入肺炎克雷伯菌后，链脲佐菌素诱导的糖尿病小鼠死亡率加速上升。糖尿病小鼠向肺泡腔募集的粒细胞较少，在气管内注入肺炎克雷伯菌脂多糖后，CXCL1、CXCL2、IL-1β和TNF-α的早期产生减少。此外，高血糖小鼠在接触肺炎克雷伯菌脂多糖后TLR2和TIRAP表达降低。这些发现表明，先天性感知受损以及未能迅速将粒细胞募集到感染部位是糖尿病患者易患呼吸道肺炎克雷伯菌感染的一种机制。
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