Abstract

Haemorrhagic fever with renal syndrome (HFRS) is characterised by an uncontrolled immune response that causes vascular leakage. Adiponectin (APN) is an adipocytokine involved in prorevascularisation and immunomodulation. To investigate the possible effects of APN in the pathogenesis of HFRS, total and high molecular weight (HMW) APN levels in the plasma of patients with HFRS were quantified using enzyme-linked immunosorbent assay (ELISA). Compared with those in healthy controls, the plasma total and HMW APN levels in patients were elevated to different degrees from the fever onset and remained high at the convalescent phase. Consistent with these results, western blot analysis additionally showed that low molecular weight (LMW), middle molecular weight (MMW), and HMW APN levels were all elevated and contributed to the elevation of the total APN level. Importantly, sustained high levels of total and HMW APN at the convalescent phase were significantly higher in patients with critical disease than those in patients with mild or moderate disease. Moreover, total and HMW APN levels negatively correlated with white blood cell count and positively correlated with platelet count and serum albumin level. These results may provide insights into understanding the roles of total and HMW APN in the pathogenesis of HFRS.

Highlights

  • Hantaan virus (HTNV) infection can cause severe haemorrhagic fever with renal syndrome (HFRS) in humans

  • The sustained high level of high molecular weight (HMW) APN in the convalescent phase was associated with disease severity, and the elevated level of HMW APN contributed to an increase in the total APN. These results suggested that both total and HMW APN may play a role after HTNV infection in HFRS patients

  • We could not obtain accurate levels of low molecular weight (LMW) plus middle molecular weight (MMW) APN by enzyme-linked immunosorbent assay (ELISA), we found that HMW APN and LMW plus LMW-ALB and MMW APN levels were elevated during the acute phase of HFRS by western blot

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Summary

Introduction

Hantaan virus (HTNV) infection can cause severe haemorrhagic fever with renal syndrome (HFRS) in humans. HFRS is an infectious disease of global concern characterised by increased vascular endothelial permeability, thrombocytopenia, and renal damage [1]. HTNV infection of endothelial cells (ECs) and HTNVinduced immunological activations of the complement system and cytokine storm, such as increased proinflammatory cytokines interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α), could induce the reorganization of the endothelial cytoskeleton and junctions and mediate an increase in EC permeability [1, 3]. Increased thrombopoiesis and platelet activation may induce intravascular coagulation and cause thrombocytopenia, the accumulation of inflammatory cells, and the release of proinflammatory cytokines in kidney tissue contributing to renal damage [4, 5]

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