XiaoHua Li1, Na Du2, Guang Xu2, Peng Zhang2, Rongjing Dang3, Yanfang Jiang4, Kaiyu Zhang5. 1. Department of Infectious Diseases, The First Hospital of Jilin University, Changchun 130021, China. Electronic address: lixiaohua2018@hotmail.com. 2. Department of Infectious Diseases, The First Hospital of Jilin University, Changchun 130021, China. 3. Key Laboratory of Zoonoses Research, Ministry of Education, The First Hospital of Jilin University, Changchun 130021, China. 4. Genetic Diagnosis Center, The First Hospital of Jilin University, Changchun 130021, China; Key Laboratory of Zoonoses Research, Ministry of Education, The First Hospital of Jilin University, Changchun 130021, China. Electronic address: yanfangjiang@hotmail.com. 5. Department of Infectious Diseases, The First Hospital of Jilin University, Changchun 130021, China. Electronic address: zhangky2000@aliyun.com.
Abstract
BACKGROUND: Hantaan virus infection causes lethal hemorrhagic fever with renal syndrome (HFRS) in humans. Little is known about how monocytes contribute to HFRS pathogenesis. In this study, we aimed to investigate changes in various monocyte subsets in HFRS patients. METHODS: A total of 41 HFRS patients and 17 age-, sex-, and ethnicity-matched healthy control subjects were included in this study. Numbers/percentages of various monocyte subsets were quantitatively determined using flow cytometry. Serum levels of interleukin (IL)-10, IL-12, and tumor necrosis factor alpha (TNF-α) were detected using a cytometric bead array (CBA). RESULTS: CD14++CD16+ intermediate monocytes were significantly higher in HFRS patients compared to healthy controls (P < 0.01), especially during the acute phase. The expression of both CD163 and CD206 on CD14++CD16+ intermediate monocytes were increased during the acute phase of HFRS (P < 0.01 and P < 0.05, respectively) when comparing the convalescent phase and healthy controls. Furthermore, the numbers of CD14++CD16+ monocytes during the acute phase, and the percentages of CD14++CD16+CD163+ monocytes in patients with severe/critical HFRS were much higher compared to patients with mild/moderate HFRS. This also positively correlated with increased levels of white blood cells (WBC), blood urea nitrogen (BUN), and creatinine (Cr). However, the percentages of CD14++CD16+CD206+monocytes were higher in mild/moderate HFRS than in severe/critical HFRS, and they negatively correlated with platelets (PLT) and Cr. CONCLUSIONS: Higher frequency of the CD14++CD16+ intermediate monocytes and increased expression of CD163+ and CD206+ markers on CD14++CD16+ monocytes were detected in patients with HFRS. The changes in the frequency of CD14++CD16+ monocytes and expression of CD163 and CD206 markers on CD14++CD16+ monocytes positively correlated with the severity of HFRS.
BACKGROUND:Hantaan virus infection causes lethal hemorrhagic fever with renal syndrome (HFRS) in humans. Little is known about how monocytes contribute to HFRS pathogenesis. In this study, we aimed to investigate changes in various monocyte subsets in HFRSpatients. METHODS: A total of 41 HFRSpatients and 17 age-, sex-, and ethnicity-matched healthy control subjects were included in this study. Numbers/percentages of various monocyte subsets were quantitatively determined using flow cytometry. Serum levels of interleukin (IL)-10, IL-12, and tumor necrosis factor alpha (TNF-α) were detected using a cytometric bead array (CBA). RESULTS:CD14++CD16+ intermediate monocytes were significantly higher in HFRSpatients compared to healthy controls (P < 0.01), especially during the acute phase. The expression of both CD163 and CD206 on CD14++CD16+ intermediate monocytes were increased during the acute phase of HFRS (P < 0.01 and P < 0.05, respectively) when comparing the convalescent phase and healthy controls. Furthermore, the numbers of CD14++CD16+ monocytes during the acute phase, and the percentages of CD14++CD16+CD163+ monocytes in patients with severe/critical HFRS were much higher compared to patients with mild/moderate HFRS. This also positively correlated with increased levels of white blood cells (WBC), blood ureanitrogen (BUN), and creatinine (Cr). However, the percentages of CD14++CD16+CD206+monocytes were higher in mild/moderate HFRS than in severe/critical HFRS, and they negatively correlated with platelets (PLT) and Cr. CONCLUSIONS: Higher frequency of the CD14++CD16+ intermediate monocytes and increased expression of CD163+ and CD206+ markers on CD14++CD16+ monocytes were detected in patients with HFRS. The changes in the frequency of CD14++CD16+ monocytes and expression of CD163 and CD206 markers on CD14++CD16+ monocytes positively correlated with the severity of HFRS.
Authors: Sindhu Vangeti; Tomas Strandin; Sang Liu; Johanna Tauriainen; Anne Räisänen-Sokolowski; Luz Cabrera; Antti Hassinen; Satu Mäkelä; Jukka Mustonen; Antti Vaheri; Olli Vapalahti; Jonas Klingström; Anna Smed-Sörensen Journal: PLoS Pathog Date: 2021-03-10 Impact factor: 6.823