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Chen Q.R.,Huazhong University of Science and Technology | Guan F.,Huazhong University of Science and Technology | Yan D.J.,Huazhong University of Science and Technology | Lei D.S.,Medicine Laboratory | And 5 more authors.
Tissue Antigens | Year: 2012

Allograft inflammatory factor-1 (AIF-1) was originally cloned from a rat heart allograft under chronic rejection. Data from many studies suggested an important role of AIF-1 in several inflammatory processes. The aim of this study was to examine the dynamic expression of AIF-1 and its association with the pathogenesis of hepatic schistosomiasis in BALB/c mice infected with S. japonicum. The expression of AIF-1 and tumour necrosis factor-alpha (TNF-α) was determined by enzyme-linked immunosorbent assay, western blot and immunohistochemistry. AIF-1 and TNF-α were overexpressed in hepatic tissues at the early stage of infection, and then diminished with the length of infection. On culturing splenocytes stimulated by soluble egg antigen for 72 h, the expression of AIF-1 in infected mice was suppressed, but TNF-α increased gradually. Our results showed that AIF-1 was overexpressed in the liver of BALB/c mice infected with S. japonicum, and the interaction between AIF-1 and TNF-α or other cytokines played an important role in the pathogenesis and progression of hepatic schistosomiasis. © 2011 John Wiley & Sons A/S. Source


Chen Q.-R.,Hubei Cancer Hospital | Chen Q.-R.,University of Texas M. D. Anderson Cancer Center | Guan F.,Huazhong University of Science and Technology | Song S.-M.,University of Texas M. D. Anderson Cancer Center | And 6 more authors.
Parasitology Research | Year: 2014

Allograft inflammatory factor-1 (AIF-1) plays an important role in various inflammatory conditions. Our previous study demonstrated that AIF-1 was over-expressed in the liver of BALB/c mice infected with Schistosoma japonicum and played significant role in the pathogenesis of schistosomiasis. The aim of this study was to focus on the effect of AIF-1 treatment on liver fibrosis and necrosis of BALB/c mice infected with S. japonicum. Seventy-two BALB/c mice were infected with cercariae of S. japonicum and then divided into three groups: AIF-1-treated group, saline-treated group, and control group. The vital signs, liver function, egg load, and hepatic pathological changes of the mice were assessed, and the levels of AIF-1 and TNF-α in the liver and spleen were measured at 5, 8, and 14 weeks postinfection. The treatment of AIF-1 on the mice infected with S. japonicum suppressed the expression of TNF-α and increased the effectiveness of AIF-1 in the liver and spleen at 14 weeks postinfection. Histopathological analysis and Masson trichrome staining for the liver tissues showed that the liver fibrosis and necrosis were alleviated previously compared with other infected mice at 14 weeks postinfection. The treatment of AIF-1 on the mice infected with S. japonicum can alleviate hepatic fibrosis and necrosis which indicate that AIF-1 use may prevent and cure the liver fibrosis. © 2014 Springer-Verlag. Source


Luan Y.,Harbin Medical University | Li G.-L.,Harbin Medical University | Duo L.-B.,Harbin Medical University | Wang W.-P.,Medicine Laboratory | And 5 more authors.
Molecular Medicine Reports | Year: 2015

The present study aimed to investigate the regulatory mechanism of the AmpC enzyme by analyzing the construction and function of AmpCR, AmpE and AmpG genes in the Dhahran (DHA)-1 plasmid of Klebsiella pneumoniae (K. pneumoniae). The production of AmpC and extended-spectrum β-lactamase (ESBL) were determined following the cefoxitin (FOX) inducing test for AmpC, preliminary screening and confirmation tests for ESBL in 10 DHA-1 plasmid AmpC enzymes of K. pneumoniae strains. AmpCR, AmpD, AmpE and AmpG sequences were analyzed by polymerase chain reaction. The pACYC184-X plasmid analysis system was established and examined by regulating the pAmpC enzyme expression. The electrophoretic bands of AmpCR, AmpD, AmpE and AmpG were expressed. Numerous mutations in AmpC + AmpR (AmpCR) and in the intergenic region cistron of AmpC-AmpR, AmpD, AmpE and AmpG were observed. The homology of AmpC and AmpR, in relation to the Morganella morganii strain, was 99%, which was determined by comparing the gene sequences of Kp1 with those of Kp17 AmpCR. The specific combination of AmpR and labeled probe demonstrated a band retarded phenomenon and established a spatial model of AmpR. All the enzyme production strains demonstrated Val93→Ala in AmpG; six transmembrane domains were found in AmpE in all strains, with the exception of Kp1 and Kp4, which had only three transmembrane segments that were caused by mutation. The DHA-1 plasmid AmpC enzymes encoded by plasmid are similar to the inducible chromosomal AmpC enzymes, which are also regulated by AmpD, AmpE, AmpR and AmpG. Source


Li G.-L.,Harbin Medical University | Duo L.-B.,Harbin Medical University | Luan Y.,Harbin Medical University | Wang C.-Y.,Medicine Laboratory | And 4 more authors.
Gene Expression | Year: 2013

We investigated the occurrence of AmpC β-lactamases among Escherichia coli and Klebsiella pneumoniae isolates and determined the genotype of plasmid-mediated AmpC β-lactamases at a medical center. The AmpC β-lactamase promoter and attenuator were amplified from chromosomal DNA of high AmpC-producing E. coli isolates and sequenced. Antibiotic screening and 3D extract tests showed the presence of AmpC β-lactamase in 3.56% of K. pneumoniae and 1.88% of E. coli isolates. Ten isolates (six K. pneumoniae and four E. coli) were positive for extended spectrum β-lactamase (ESBL) as indicated by the double disc diffusion method. DHA-1 plasmid-encoded AmpC β-lactamase was present in 10 K. pneumoniae isolates and four E.coli isolates. E. coli chromosomal AmpC β-lactamase carried polymorphisms in the -42, -32, and -18 bases of the promoter and in the +26 and +27 bases of the attenuator, which may play a role in antibiotic resistance. The observed mutations may have clinical implications for the management of antibiotic-resistant infections. Copyright © 2013 Cognizant Comm. Corp. Source

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