Neumann Laura, Mueller Mattea, Moos Verena, Heller Frank, Meyer Thomas F, Loddenkemper Christoph, Bojarski Christian, Fehlings Michael, Doerner Thomas, Allers Kristina, Aebischer Toni, Ignatius Ralf, Schneider Thomas
Medical Clinic I, Gastroenterology, Infectious Diseases and Rheumatology, Charité-University Medicine Berlin, 12203 Berlin, Germany;
Practice for Gastroenterology, 12163 Berlin, Germany;
J Immunol. 2016 Sep 1;197(5):1801-8. doi: 10.4049/jimmunol.1501330. Epub 2016 Jul 25.
The mucosal immune system is relevant for homeostasis, immunity, and also pathological conditions in the gastrointestinal tract. Inducible NO synthase (iNOS)-dependent production of NO is one of the factors linked to both antimicrobial immunity and pathological conditions. Upregulation of iNOS has been observed in human Helicobacter pylori infection, but the cellular sources of iNOS are ill defined. Key differences in regulation of iNOS expression impair the translation from mouse models to human medicine. To characterize mucosal iNOS-producing leukocytes, biopsy specimens from H. pylori-infected patients, controls, and participants of a vaccination trial were analyzed by immunohistochemistry, along with flow cytometric analyses of lymphocytes for iNOS expression and activity. We newly identified mucosal IgA-producing plasma cells (PCs) as one major iNOS(+) cell population in H. pylori-infected patients and confirmed intracellular NO production. Because we did not detect iNOS(+) PCs in three distinct infectious diseases, this is not a general feature of mucosal PCs under conditions of infection. Furthermore, numbers of mucosal iNOS(+) PCs were elevated in individuals who had cleared experimental H. pylori infection compared with those who had not. Thus, IgA(+) PCs expressing iNOS are described for the first time, to our knowledge, in humans. iNOS(+) PCs are induced in the course of human H. pylori infection, and their abundance seems to correlate with the clinical course of the infection.
黏膜免疫系统与胃肠道的内环境稳定、免疫以及病理状况相关。诱导型一氧化氮合酶(iNOS)依赖性一氧化氮的产生是与抗微生物免疫和病理状况相关的因素之一。在人类幽门螺杆菌感染中已观察到iNOS的上调,但iNOS的细胞来源尚不明确。iNOS表达调控的关键差异阻碍了从小鼠模型到人类医学的转化。为了表征产生黏膜iNOS的白细胞,我们通过免疫组织化学分析了幽门螺杆菌感染患者、对照以及疫苗试验参与者的活检标本,并对淋巴细胞进行了流式细胞术分析以检测iNOS的表达和活性。我们新发现黏膜产生IgA的浆细胞(PCs)是幽门螺杆菌感染患者中一个主要的iNOS(+)细胞群体,并证实了细胞内一氧化氮的产生。由于我们在三种不同的传染病中未检测到iNOS(+)浆细胞,所以这不是感染条件下黏膜浆细胞的普遍特征。此外,与未清除实验性幽门螺杆菌感染的个体相比,清除了感染的个体中黏膜iNOS(+)浆细胞的数量有所增加。因此,据我们所知,人类中首次描述了表达iNOS的IgA(+)浆细胞。iNOS(+)浆细胞在人类幽门螺杆菌感染过程中被诱导,其丰度似乎与感染病程相关。