Abstract
Human parvovirus B19 (B19) has been associated with a variety of diseases. However, the influence of B19 viral proteins on hepatic injury in SLE is still obscure. To elucidate the effects of B19 viral proteins on livers in SLE, recombinant B19 NS1, VP1u or VP2 proteins were injected subcutaneously into NZB/W F1 mice, respectively. Significant expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were detected in NZB/W F1 mice receiving B19 NS1 as compared to those mice receiving PBS. Markedly hepatocyte disarray and lymphocyte infiltration were observed in livers from NZB/WF 1 mice receiving B19 NS1 as compared to those mice receiving PBS. Additionally, significant increases of Tumor Necrosis Factor –α (TNF-α), TNF-α receptor, IκB kinase –α (IKK-α), nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor (IκB) and nuclear factor-kappa B (NF-κB) were detected in livers from NZB/W F1 mice receiving B19 NS1 as compared to those mice receiving PBS. Accordingly, significant increases of matrix metalloproteinase-9 (MMP9) and U-plasminogen activator (uPA) were also detected in livers from NZB/W F1 mice receiving B19 NS1 as compared to those mice receiving PBS. Contrarily, no significant variation on livers from NZB/W F1 mice receiving B19 VP1u or VP2 was observed as compared to those mice receiving PBS. These findings firstly demonstrated the aggravated effects of B19 NS1 but not VP1u or VP2 protein on hepatic injury and provide a clue in understanding the role of B19 NS1 on hepatic injury in SLE.
Highlights
Systematic lupus erythematosus (SLE) is known as a systemic autoimmune disorder that affects various organs including liver [1]
Human parvovirus B19 has been strongly associated with the pathogenesis of SLE
Significant increase of COX-2 protein was detected in livers from NZB/W F1 mice receiving B19-NS1 whereas no significant variation on COX-2 expression in livers from NZB/W F1 receiving B19-VP1u or VP2 was observed as compared to those mice receiving phosphate-buffered saline (PBS) (Fig. 1B)
Summary
Systematic lupus erythematosus (SLE) is known as a systemic autoimmune disorder that affects various organs including liver [1]. Various reports have indicated that growing population with liver disease was found in patients with SLE [2,3,4]. The occurrence of liver disease is not routinely screened, the incidence of hepatic abnormality in patients with SLE was reported as varying from 12% to 55% [4]. A clinical study reported the existence of B19 DNA in a liver biopsy specimen from a patient with acute hepatitis [9]. Another studies suggested an important role of B19 infection in acute icteric hepatitis liver injury [10] and acute fulminant hepatitis with bone marrow failure [11]. B19 infection has been recognized to trigger the acute liver failure in a patient with Wilson disease [12]
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