Macrophage migration inhibitory factor levels are associated with disease activity and possible complications in membranous nephropathy.

Membranous nephropathy (MN) is an autoimmune disease characterized by the deposition of immunoglobulin G (IgG) and complementary components in the epithelium of the glomerular capillary wall. Macrophage migration inhibitory factor (MIF) is an inflammatory mediator released by macrophages. MIF plays a key regulatory function in the pathogenesis of immune-mediated glomerulonephritis.

Macrophage migration inhibitory factor contributes to anti-neutrophil cytoplasmic antibody-induced neutrophils activation.

Background: Macrophage migration inhibitory factor (MIF) is an inflammatory mediator released by macrophages that is central to the innate immune system, with an upstream role in the inflammatory cascade. MIF is one of the most important pathogenic factors in the development of the autoimmune diseases. In the current study, we investigated the role of MIF in anti-neutrophil cytoplasmic antibody (ANCA)-induced neutrophil activation.

Association of IP-10 gene polymorphism with susceptibility to Enterovirus 71 infection.

Enterovirus 71 (EV71) often causes large outbreaks of diseases among children worldwide and its pathogenesis remains unclear. The aim of the present study was to investigate the association between interferon-inducible protein 10 (IP-10) polymorphism in children with EV71 infection. Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) were performed to analyze the gene polymorphisms of IP-10 (-1596C/T) in 58 EV71-infected and 48 control patients.

Genetic polymorphism of CCL2-2518, CXCL10-201, IL8+781 and susceptibility to severity of Enterovirus-71 infection in a Chinese population.

Objective: The goal of this study was to examine the relationship between CCL2-2518A/G, CXCL10-201A/G, and IL8+781C/T gene polymorphism and severity of Enterovirus 71 (EV71) infection in a Chinese population.

Methods: A case-control study was conducted to compare the distribution of genotype and genetic frequency of the CCL2-2518A/G, CXCL10-201A/G, and IL8+781C/T gene polymorphisms among EV71-infected patients (n = 186), including mild cases (n = 103), severe cases (n = 83) and healthy control subjects (n = 233) with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and analyzed the relationship between the CCL2-2518A/G, CXCL10-201A/G, and IL8+781C/T gene polymorphism and the susceptibility to EV71 infection.

Results: No significant differences were found in the distribution of genotype CCL2-2518A/G, CXCL10-201A/G, and IL8+781C/T between the healthy control group and EV71-infected patients.

Impact of endothelial nitric oxide synthase gene polymorphism on severity of enterovirus 71-infection in Chinese children.

Objectives: Genetic polymorphism G894T on the endothelial nitric oxide synthase (eNOS) gene has been reported as a susceptibility factor in a number of diseases, but evidence of its effect on enterovirus 71 (EV71) infection is lacking. This study investigated the possible association between this polymorphism (rs1799983) and disease severity in Chinese children with EV71 infection.

Design And Methods: 185 children with EV71 infection (83 with severe and 102 with mild disease) and 234 control healthy children underwent testing with polymerase chain reaction-restriction fragment length polymorphism (PCR-RLFP) to detect G894T polymorphism.

Association of interleukin 10 and interferon gamma gene polymorphisms with enterovirus 71 encephalitis in patients with hand, foot and mouth disease.

Enterovirus 71 (EV71) is one of the common causative agents of hand, foot and mouth disease (HFMD), and is associated with several outbreaks with neurological complications including encephalitis. This study investigated the polymorphisms of interferon gamma (IFN-γ)+874 T/A and interleukin 10 (IL-10)-1082 G/A in 65 Chinese patients with EV71 encephalitis and 113 Chinese HFMD patients without complications. The polymorphisms of IFN-γ+874 T/A and IL-10-1082 G/A were determined by polymerase chain reaction (PCR)-amplification refractory mutation system (ARMS) and PCR-sequence-specific primer (SSP) analysis, respectively.