Effects of recombinant fusion protein interleukin-18 on expression of immune-inflammatory factors in mice infected with Staphylococcus aureus / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To observe the effects of recombinant fusion protein interleukin (IL)-18 on the expression of immune-inflammatory factors in the mice infected with Staphylococcus aureus (SA), and to investigate the mechanism of action of IL-18 in defense of SA infection in vivo.</p><p><b>METHODS</b>A total of 40 specific pathogen-free female BLAB/c mice were randomly divided into four groups: control, SA infection, immunized, and intervention. A mouse model of SA infection was established by nasal inoculation with SA liquid. The immunized group and the intervention group were intranasally given IL-18 before SA modeling, and then the SA infection group and the intervention group received the nasal inoculation with SA liquid; the control group was treated with phosphate buffered saline instead. The levels of IL-4, interferon (IFN)-γ, tumor necrosis factor (TNF), granulocyte colony-stimulating factor (G-CSF), IgM in the serum and bronchoalveolar lavage fluid (BALF) of mice were measured by enzyme-linked immunosorbent assay. The expression of macrophage inflammatory protein (MIP)-1α mRNA and MIP-2β mRNA in the lung tissue of mice were determined by real-time fluorescent quantitative PCR.</p><p><b>RESULTS</b>Compared with the control group, the SA infection group and the immunized group had significantly higher levels of IL-4, G-CSF, and IgM in the serum and BALF and expression of MIP-1α mRNA and MIP-2β mRNA in the lung tissue (P<0.05); the SA infection group had a significantly lower level of IFN-γ and a significantly higher level of TNF in the serum and BALF (P<0.05); the immunized group had a significantly higher level of IFN-γ in the serum and BALF (P<0.05). Compared with the SA infection group, the intervention group had significantly higher levels of IL-4, IFN-γ, G-CSF, and IgM in the serum and BALF and expression of MIP-1α mRNA in the lung tissue. In contrast, the intervention group showed a significantly lower level of TNF in the serum and BALF and expression of MIP-2β mRNA in the lung tissue (P<0.05). All the above indicators in the intervention group were significantly higher than those in the control group (P<0.05), except the serum level of IFN-γ.</p><p><b>CONCLUSIONS</b>In the mice infected with SA, the recombinant fusion protein IL-18 by mucosal immunity can affect inflammatory factors in the serum and BALF and the expression of MIP-1α mRNA and MIP-2β mRNA in the lung tissue to promote the anti-infective immune response and enhance the ability to clear pathogens.</p>

The protective effect of N-acetylcysteine magnesium against liver cirrhosis with portal hypertension in rat / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>To study the effects of acetylcysteine magnesium on the vasoactive substances and hepatic fibrosis indexes in liver cirrhosis and portal hypertension of rats.</p><p><b>METHODS</b>The rat liver cirrhosis model was made with 12 microg/kg dimethylnitrosamines. Then acetylcysteine magnesium was injected respectively with 25, 50, and 100 mg x kg(-1) dose daily into abdominal cavity. After 8 weeks treatment, pathological section, TGF-beta1, NO, TNOS and iNOS of hepatic tissue were detected to assess the effect of acetylcysteine magnesium against cirrhosis portal hypertension.</p><p><b>RESULTS</b>After the DMNA modeling was completed, the HE and Sweet reticulocyte staining of liver pathological section showed that cirrhosis of the liver was in the III-IV phase, the infiltration of lymphocytes and formation of pseudolobuli in liver were alleviated in three acetylcysteine magnesium treatment groups (low, medium, and high dose), and the degree of liver fiber sclerosis in three groups was significantly lower than control group. Compared with control group, TGF-beta1, NO, TNOS and iNOS were significantly reduced in all treatment groups (P < 0.05).</p><p><b>CONCLUSION</b>Acetylcysteine magnesium is probably a distinctive antioxidant which can remove various free radical in body and modulate ligand-dependent signal transduction and the growth of cell. It also have protection in the liver cirrhosis and portal hypertension of rats induced by dimethylnitrosamine.</p>

Correlation between-173 G/C Gene Polymorphism of Macrophage Migration Inhibitory Factor and Henoch-Schonlein Purpura Nephritis / 实用儿科临床杂志

Objective To explore the correlation between-173G/C gene polymorphism of macrophage migration inhibitory factor(MIF) and Henoch-Schonlein purpura(HSP),Henoch-Schonlein purpura nephritis(HSPN) in children in Jiangxi Province.Methods One hundred and thirty-one ethnic Han children with HSP were enrolled,including 80 children with concurrent nephritis(HSPN group) and 51 children without nephritis(HSP without nephritis group).One hundred and five healthy children were used as the healthy control group.Germline DNA was extracted from peripheral blood by Promega blood genomic DNA kit.Polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) was used for genotyping the-173G/C polymorphism of MIF.Genotype distribution and allele frequencies were obtained by direct counting.Statistical analysis was performed by using SPSS 11.5 software.Allele and genotype distribution were compared by using the chi-square test.The relative risk of allele was described by odds ratios(OR) and 95% confidence intervals(95%CI).Results Three genotypes(GG,GC,CC) were detected in MIF-173 G/C.GG,GC genotypes were detected in HSP without nephritis and healthy control group.GG,GC and CC genotypes were detected in HSPN group.Mutant genotype(37.5%) and C allele frequency(20.0%) in HSPN group were significantly higher than those in healthy control group(20.0% and 10.0%,respectively)(?2=6.964,7.400,Pa