Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Guldhedsgatan 10A, 413 46, Gothenburg, Sweden.
Department of Clinical Microbiology, Sahlgrenska University Hospital, Gothenburg, Region Västra Götaland, Sweden.
Med Microbiol Immunol. 2022 Jun;211(2-3):133-141. doi: 10.1007/s00430-022-00737-6. Epub 2022 Apr 17.
The tick-borne bacterium Neoehrlichia mikurensis causes the infectious disease neoehrlichiosis in humans. Vascular endothelium is one of the target cells of the infection. Neoehrlichiosis patients with compromised B cell immunity present with more severe inflammation than immunocompetent patients. The aim of this study was to compare the cytokine profiles of immunocompetent and immunosuppressed patients with neoehrlichiosis.
Blood samples from Swedish and Norwegian immunosuppressed (N = 30) and immunocompetent (N = 16) patients with neoehrlichiosis were analyzed for the levels of 30 cytokines, using a multiplex cytokine assay and ELISA. A gender-matched healthy control group (N = 14) was analyzed in parallel. Data were analyzed using the multivariate method OPLS-DA.
The multiplex cytokine analyses generated more cytokine results than did the uniplex ELISA analyses. Multivariate analysis of the multiplex cytokine results established that increased levels of FGF2, GM-CSF, CXCL10, and IFN-γ were associated with immunosuppressed patients, whereas increased levels of IL-15 and VEGF were associated with immunocompetent neoehrlichiosis patients. When multivariate analysis findings were confirmed with uniplex ELISA, it was found that both groups of patients had similarly elevated levels of VEGF, FGF2 and IFN-γ. In contrast, the immunosuppressed patients had clearly elevated levels of CXCL10, CXCL13 and BAFF, whereas the immunocompetent patients had the same levels as healthy controls.
Pro-angiogenic and type 1 cytokines were produced as part of the host response of neoehrlichiosis independent of immune status, whereas immunosuppressed neoehrlichiosis patients produced cytokines required for B cell-mediated defense.
蜱传细菌嗜吞噬细胞无形体引起人类传染病无形体病。血管内皮细胞是感染的靶细胞之一。B 细胞免疫受损的无形体病患者比免疫功能正常的患者表现出更严重的炎症。本研究旨在比较免疫功能正常和免疫抑制患者无形体病的细胞因子谱。
分析来自瑞典和挪威免疫抑制（N=30）和免疫功能正常（N=16）无形体病患者的血液样本中的 30 种细胞因子水平，使用多重细胞因子分析和 ELISA。同时分析了性别匹配的健康对照组（N=14）。使用多元方法 OPLS-DA 分析数据。
多重细胞因子分析产生的细胞因子结果多于单重 ELISA 分析。多重细胞因子分析的多元分析确定，FGF2、GM-CSF、CXCL10 和 IFN-γ水平升高与免疫抑制患者有关，而 IL-15 和 VEGF 水平升高与免疫功能正常的无形体病患者有关。当使用单重 ELISA 验证多元分析结果时，发现两组患者的 VEGF、FGF2 和 IFN-γ水平均升高。相比之下，免疫抑制患者的 CXCL10、CXCL13 和 BAFF 水平明显升高，而免疫功能正常的患者与健康对照组的水平相同。
在不依赖免疫状态的情况下，作为无形体病宿主反应的一部分产生了促血管生成和 1 型细胞因子，而免疫抑制的无形体病患者产生了 B 细胞介导防御所需的细胞因子。
