Wasbotten Rachel K, Dahler Aubree A, Mackel Joseph J, Morffy Smith Catherine, Rosen David A
Department of Pediatrics, Division of Pediatric Infectious Diseases, Washington University School of Medicine, St. Louis, Missouri, USA.
Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri, USA.
Infect Immun. 2022 Apr 21;90(4):e0059621. doi: 10.1128/iai.00596-21. Epub 2022 Mar 21.
Klebsiella pneumoniae is a Gram-negative, opportunistic pathogen that commonly causes nosocomial pneumonia, urinary tract infection, and septicemia. Our recent work utilizing a murine model of respiratory tract infection with classical K. pneumoniae demonstrated leukocyte aggregates in the lungs of mice at 28 days postinfection. Here, we sought to characterize the composition and development of these structures. Histopathological analyses of murine lungs revealed immune cell clusters surrounding the pulmonary vasculature and airways by 14 days postinfection, resembling inducible bronchus-associated lymphoid tissue (iBALT). Further investigation of these structures demonstrated central B cell aggregates with concomitant dispersed T cells. At day 28 postinfection, these lymphoid clusters expressed germinal center markers and CXCL12, qualifying these structures as iBALT with nonclassical B cell follicles. Investigations in mutant mice revealed that those lacking B and/or T cells were not able to form fully defined iBALT structures, although some rudimentary B cell clusters were identified in mice lacking T cells. The longevity of K. pneumoniae-induced BALT was assessed for up to 120 days postinfection. Lymphoid aggregates significantly decreased in size and quantity by 90 days after K. pneumoniae infection; however, aggregates persisted in mice that were restimulated with K. pneumoniae every 30 days. Finally, infections of mice with an array of classical K. pneumoniae clinical isolates demonstrated that the development of these structures is a common feature of K. pneumoniae lung infection. Together, these data confirm that murine lungs infected with K. pneumoniae develop iBALT, which may play a role in pulmonary immunity to this troublesome pathogen.
肺炎克雷伯菌是一种革兰氏阴性机会致病菌,通常会引起医院获得性肺炎、尿路感染和败血症。我们最近利用经典肺炎克雷伯菌呼吸道感染小鼠模型的研究表明,感染后28天小鼠肺部出现白细胞聚集。在此,我们试图对这些结构的组成和发育进行表征。对小鼠肺部的组织病理学分析显示,感染后14天,肺血管和气道周围出现免疫细胞簇,类似于诱导性支气管相关淋巴组织(iBALT)。对这些结构的进一步研究表明,中央有B细胞聚集,同时T细胞分散分布。感染后第28天,这些淋巴簇表达生发中心标志物和CXCL12,将这些结构定性为具有非经典B细胞滤泡的iBALT。对突变小鼠的研究表明,缺乏B细胞和/或T细胞的小鼠无法形成完全明确的iBALT结构,尽管在缺乏T细胞的小鼠中发现了一些原始的B细胞簇。在感染后长达120天的时间里评估了肺炎克雷伯菌诱导的BALT的寿命。肺炎克雷伯菌感染后90天,淋巴聚集物的大小和数量显著减少;然而,在每30天用肺炎克雷伯菌重新刺激的小鼠中,聚集物仍然存在。最后,用一系列经典肺炎克雷伯菌临床分离株感染小鼠表明,这些结构的发育是肺炎克雷伯菌肺部感染的一个共同特征。总之,这些数据证实,感染肺炎克雷伯菌的小鼠肺部会形成iBALT,其可能在针对这种麻烦病原体的肺部免疫中发挥作用。