title: Effect of Ipr1 on expression levels of immune genes related to macrophage anti-infection of mycobacterium tuberculosis.
abstract: BACKGROUND
  Intracellular pathogen resistance 1 (Ipr1) has been found in macrophages and plays a pivotal role in fighting against Mycobacterium tuberculosis (Mtb) infection. This study is designed to evaluate the effect of Iprl on the expression of macrophage genes related to the anti-infection of Mtb. Design or methods: In the experimental and control groups, the macrophages were infected with Mycobacterium H37Ra, and then the related immune genes between two groups were detected using microarray assay. Real-time quantitative PCR was applied to detect the differences in the expression of three up-regulated genes detected by microarray assay and to verify the reliability of microarray assay.
  
  
  RESULTS
  The expression of Iprl up-regulated 11 genes related to macrophage anti-immunity involved TLRs signaling pathway including TLR2 and TLR4, Irak1, Traf7, Ifngr1 and Tnfrsfla. No significant difference was found in terms of the molecular expression involved in regulation of the adaptive immune response, such as IL-1 and IL-12. The results of real-time PCR were consistent with the findings of microarray assay.
  
  
  CONCLUSIONS
  The expression of Iprl gene probably promotes macrophage activity and enhances the ability of macrophages to fight against Mtb infection. The underlying mechanism may be achieved by up-regulating the expression levels of innate immunity genes, especially TLR2/TLR4 and signal transduction molecules, which is determined using microarray assay. All these findings offer the basis for subsequent study of the mechanisms of Ipr1 gene in host innate immunity against Mtb infection.
authors.affiliation: Department of Nuclear Medicine, The Affiliated Hospital of Binzhou Medical University Binzhou 256600.
authors.forename: Na
authors.initials: N
authors.lastname: Li
authors.affiliation: Department of Neurosurgery, The Affiliated Hospital of Binzhou Medical University Binzhou 256600.
authors.forename: Pengfei
authors.initials: P
authors.lastname: Liu
authors.affiliation: Department of Nuclear Medicine, The Affiliated Hospital of Binzhou Medical University Binzhou 256600.
authors.forename: Lianwen
authors.initials: L
authors.lastname: Wang
authors.affiliation: Department of Nuclear Medicine, The Affiliated Hospital of Binzhou Medical University Binzhou 256600.
authors.forename: Jingbo
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Nuclear Medicine, The Affiliated Hospital of Binzhou Medical University Binzhou 256600.
authors.forename: Xiao
authors.initials: X
authors.lastname: Yuan
authors.affiliation: Department of Clinical Laboratory, The Affiliated Hospital of Binzhou Medical University Binzhou 256600.
authors.forename: Wei
authors.initials: W
authors.lastname: Meng
authors.affiliation: Department of Clinical Laboratory, The Affiliated Hospital of Binzhou Medical University Binzhou 256600.
authors.forename: Yan
authors.initials: Y
authors.lastname: Dong
authors.affiliation: Department of Pathogeny Biology, Binzhou Medical University Yantai 264003.
authors.forename: Boqing
authors.initials: B
authors.lastname: Li
keywords: Iprl; gene expression; innate immunity; macrophages; mycobacterium tuberculosis