Objective To observe the expressions of RANTES , FKN and IP-10 at mRNA and pro-tein levels in human lung epithelial cells (A549) infected by respiratory syncytial virus (RSV), and to eval-uate the changes of them interfered with 15-deoxy-delta12,14prostaglandin J2(15d-PGJ2), rosiglitazone or 2-chloro-5-nitrobenzanilide ( GW9662 ) .Methods A549 cells were seeded in 6-well culture plates and cul-tured overnight in F12K culture solution.Then they were randomly divided into five groups , including group A (15d-PGJ2+RSV group), group B (rosiglitazone+RSV group), group C (DMSO+RSV group), group D (GW9662+rosiglitazone+RSV group) and group E (cell control group).Cells and supernatants were harves-ted from each group at different time points (12 h, 24 h and 48 h) of culture.The expressions of RANTES , FKN and IP-10 at mRNA and protein levels were measured by ELISA and real-time quantitative RT-PCR analysis.Results The expressions of RANTES , FKN and IP-10 at mRNA and protein levels in group C were significantly higher than those in group E at time points of 12 h, 24 h and 48 h (all P<0.05).In group C, the expressions of the three chemokines at mRNA level reached a peak at 24 h, but began to de-crease at 48 h, which showed no statistical significance compared with those at 12 h (all P>0.05).Moreo-ver, the expressions at protein level were peaked at 48h, and had significant difference with those expressed at 12 h and 24 h (all P<0.05).Compared with group C, the expressions of the three chemokines both at mRNA level and protein level were decreased in group A and B as the dose was increased (all P<0.05), and the lowest levels were observed with the intervention of 20 μmol/L of 15d-PGJ2 in group A and 30μmol/L of rosiglitazone in group B .Conclusion The expressions of RANTES , FKN and IP-10 at mRNA and protein levels were increased with RSV infection , and the peaks of mRNA level and protein level were respectively achieved at 24 h and 48 h after infection.PPARγagonists played an anti-inflammatory role through inhibiting the expressions of the three chemokines both at mRNA level and protein level in a dose -de-pendent manner .

Objective To investigate the correlation between ADAM33 T1, S2 gene polymorphism and Bronchial asthma risk in china. Methods We retrived the relevant published studies about ADAM33 T1, S2 gene polymorphism and bronchial asthma risk. Then we divided the population into Chinese and other Asian population. Odds ratio (OR) of Case group and control group was selected as the effect index. Stata 11.0 software was used to calculate heterogeneity test, ORs and 95%CI of two areas, and gave the forest plot and funnel plot of meta results. Results A total of 27 studies were included in this analysis,18 studies in ADAM33 T1 site were 3881 cases in case group, and 3780 cases in control group;and 14 studies in ADAM33 S2 site were 3222 cases in case group, and 3513 cases in control group. Additive model, dominant model, recessive model of ADAM33 T1 in Chinese had association with the susceptibility of bronchial asthma. The results were OR=1.488, 95% CI:1.002-2.167 in Additive model, OR=1.619, 95%CI:1.059-2.475 in dominant model;OR=2.523, 95%CI:1.910-3.333 in recessive model. Three models of ADAM33 T1 in other Asian country had no association with the susceptibility of Bronchial Asthma. Three gene model of ADAM33 S2 in Asian had no association with bronchial asthma susceptibility. Except ADAM33 T1 polymorphism in recessive model, other mode of T1, S2 had no publication bias in Chinese population. Conclusion There are association between ADAM33 T1 gene polymorphism and bronchial asthma, but ADAM33 S2 gene polymorphism and bronchial asthma have no association in Chinese population.

Objective To explore whether IL-27 inhibited the pulmonary fibrosis through regulating the expression of TGF-β/Smad signaling pathway in the bleomycin-induced pulmonary fibrosis model. Methods Forty male C57/BL6 mice were randomly divided into normal control group(group A),bleomycin-induced pulmonary fibrosis group(group B),bleomycin+IL-27 group(group C)and bleomycin+IL-27 antibody group(group D) with 10 in each. Five mice in each group were sacrificed on days 7 and 28 after with intratracheal bleomycin. TGF-βR1,Smad1 and Smad3 in right lung tissue were measured by Western Blot. Results 1. In the bleomycin-induced pulmonary fibrosis model,the expression of TGF-βR1 was higher on days 7 and 28,which was inhibited by IL-27. 2. The expressions of p-Smad1 and p-Smad3 were highest in group D on days 7 and 28, but were lower in group C on day 7 than those in group B. Conclusion Exogenous IL-27 might alleviate pulmonary fibrosis through inhibiting the related protein phosphorylation in TGF-β/Smad signaling pathway.

OBJECTIVETo investigate the effects of interleukin-17 (IL-17) on the proliferation, transformation and collagen synthesis of the lung fibroblasts in mice with bleomycin-induced pulmonary fibrosis.

METHODSIn a mouse model of pulmonary fibrosis established by intratracheal administration of 5 mg/kg bleomycin, the dynamic expressions of IL-17/IL-17 receptor (IL-17R) mRNAs were detected by RT-PCR. At 14 days following bleomycin administration, the pulmonary fibroblasts were isolated, cultured and identified. MTT assay was used to assess the proliferation of the pulmonary fibroblasts in response to IL-17 treatment at different concentrations, and RT-PCR and Western blotting were employed to examine the mRNA and protein expressions of α-smooth muscle actin (α-SMA) and types I and III collagen.

RESULTSIL-17/IL-17R mRNA levels were increased obviously in the pulmonary fibroblasts of rats with pulmonary fibrosis, and the highest expressions occurred at 14 days following bleomycin administration. Exogenous IL-17, at the optimal concentration of 50 ng/ml, significantly promoted the proliferation of the pulmonary fibroblasts in primary culture and obviously increased α-SMA expression and types I and III collagen synthesis in the fibroblasts.

CONCLUSIONIL-17 can promote the proliferation, transformation, and collagen synthesis of the pulmonary fibroblasts from rats with bleomycin-induced pulmonary fibrosis.

Animals ; Bleomycin ; Cell Proliferation ; Cells, Cultured ; Collagen Type I ; biosynthesis ; Collagen Type III ; biosynthesis ; Epithelial-Mesenchymal Transition ; Fibroblasts ; metabolism ; pathology ; Interleukin-17 ; genetics ; metabolism ; Lung ; pathology ; Male ; Mice ; Mice, Inbred C57BL ; Pulmonary Fibrosis ; chemically induced ; metabolism ; pathology ; RNA, Messenger ; genetics ; metabolism ; Receptors, Interleukin-17 ; genetics ; metabolism

OBJECTIVEGroup A β-hemolytic streptococcus (GAS) or Streptococcus pyogenes may be encountered in diverse clinical situations in children. A rising incidence of invasive group A streptococcus (IGAS) infections has been noted in children in the past three decades. The aim of this study was to summarize the clinical characteristics and antimicrobial resistance of IGAS in children, and to raise the level of diagnosis and treatment of this infection.

METHODThe clinical data from 19 cases of IGAS younger than 14 years old seen from January 2004 to December 2011 treated in the authors' hospital were analyzed. IGAS infections are defined as the isolation of GAS from a normally sterile site in patients.

RESULTThe 19 cases were identified as IGAS infections, among whom 15 were male and 4 were female, and the ratio of them was 3.75. The age ranged from 1 day to 14 years, with a median age of 4 years. The course of disease was 4 h-10 days. The average length of stay was 12.2 days. In 13 cases the episodes of the infection occurred in winter and spring. In 18 cases the infection was community-acquired. Overall, 10 cases had neck or foot dorsum abscess, four cases had purulent peritonitis, and 3 cases were diagnosed as streptococcal toxic shock syndrome (STSS) complicated with empyema, pyopneumothorax occurred in 1 case and neonatal septicemia in another. Three cases had an underlying disease, including 2 cases wounded in a car accident and 1 case of congenital esophageal atresia and tracheoesophageal fistula. Before the isolation of GAS, 5 cases had stayed in ICUs, the length of ICU stay was 1-32 days, 4 cases had received intubation and mechanical ventilation, the ventilation time was 8 h-24 days, 2 cases had received major surgery; 5 cases had other pathogen coinfection, including 4 cases of abdominal pus at the same time and Escherichia coli was isolated, and 1 case had parainfluenza virus type I coinfection. Peripheral blood leucocyte increased in 18 cases, one case dropped off. The C-reactive protein (CRP) levels increased in all patients, including 16 cases who had 14-160 mg/L, 3 cases had levels higher than 160 mg/L. Twenty strains of GAS were isolated from 19 cases' sterile sites, of them 10 strains were isolated from abscess, 4 strains were isolated from blood and another 4 from ascites. Two strains were from the same patient at different times of pleural effusion. All 20 strains displayed a full susceptibility to cefazolin, levofloxacin and vancomycin, and the rates of resistance to both cefotaxime and penicillin were 10.0%. The rates of resistance to erythromycin and clindamycin were 55.0% and 70.0% respectively. Among the patients 3 cases were cured, 14 cases improved, and 2 cases died, of whom 1 case died of STSS secondary to multiple organ dysfunction, 1 case died of basic disease secondary to multiple organ dysfunction.

CONCLUSIONSkin and soft tissues were the most common IGAS infection sites in children, and IGAS infection also can lead to serious STSS and even can be life threatening. Penicillin and cephalosporin are still sensitive for children IGAS infections.

Abscess ; drug therapy ; epidemiology ; microbiology ; Adolescent ; Anti-Bacterial Agents ; pharmacology ; therapeutic use ; Cephalosporins ; therapeutic use ; Child ; Child, Preschool ; Clindamycin ; therapeutic use ; Community-Acquired Infections ; drug therapy ; epidemiology ; microbiology ; Drug Resistance, Bacterial ; Female ; Humans ; Infant ; Infant, Newborn ; Male ; Microbial Sensitivity Tests ; Retrospective Studies ; Soft Tissue Infections ; drug therapy ; epidemiology ; microbiology ; Streptococcal Infections ; drug therapy ; epidemiology ; microbiology ; Streptococcus pyogenes ; drug effects ; isolation & purification

OBJECTIVEThe purpose of this study was to investigate the effect and mechanism of Vav3 gene on the proliferation of human gastric cancer cell line SGC7901.

METHODSThe expressions of Vav3 proten in gastric cancer tissue, tumor-adjacent tissue, human gastric cancer cell line SGC7901 and gastric epithelial cell line GES-1 cells were tested by Western blot. Vav3-siRNA was transfected into the SGC7901 cells. The proliferation of SGC7901 cells in vitro was measured by MTT assay. Cell cycle of SGC7901 cells was determined by flow cytometry.The expressions of proliferation-related genes PCNA, p16, cyclin D1, Rb were determined by qPCR and Western blot assay. Orthotopic transplantation nude mouse models of gastric cancer were prepared, and the tumor growth and expressions of PCNA, P16, cyclin D1, and Rb proteins were examined.

RESULTSThe relative expressions of Vav3 in the gastric cancer and peritumoral tissue were 0.910±0.242 and 0.243±0.045, respectively; the relative expressions of Vav3 in SGC7901 and GSE-1 cells were 0.925±0.127 and 0.277±0.038, respevtively (both P<0.05). The expression of Vav3 protein in SGC7901 cells was effectively inhibited by Vav3-siRNA. Proliferation of SGC7901 cells was inhibited by (83.43±10.17)% after 80 nmol/L Vav3-siRNA transfection (P<0.05). The ratio of SGC7901 cells in G0/G1 phase was increased, and in S phase decreased after Vav3-siRNA transfection (both P<0.05). The expressions of PCNA and cyclin D1 were decreased in cells after Vav3-siRNA transfection, and expressions of p16 and Rb were increased after Vav3-siRNA transfection (P<0.05 for all). The tumor growth in the Vav3-siRNA group was much slower than that in the other 2 control groups of nude mouse models. Compared with the two control groups, expressions of PCNA and cyclin D1 were significantly lower in the Vav3-siRNA group, while expressions of p16 and Rb were increased (P<0.05 for all).

CONCLUSIONVav3 can promote the proliferation of gastric cancer cells by regulating proliferation-related genes.

Animals ; Cell Cycle ; Cell Line, Tumor ; Cell Proliferation ; Cyclin D1 ; metabolism ; Humans ; Mice ; Mice, Nude ; Proto-Oncogene Proteins c-vav ; metabolism ; RNA, Small Interfering ; Stomach Neoplasms ; metabolism ; Transfection