title: Identification of gene networks and pathways associated with Guillain-Barré syndrome.
abstract: BACKGROUND
  The underlying change of gene network expression of Guillain-Barré syndrome (GBS) remains elusive. We sought to identify GBS-associated gene networks and signaling pathways by analyzing the transcriptional profile of leukocytes in the patients with GBS.
  
  
  RESULTS
  Quantitative global gene expression microarray analysis of peripheral blood leukocytes was performed on 7 patients with GBS and 7 healthy controls. Gene expression profiles were compared between patients and controls after standardization. The set of genes that significantly correlated with GBS was further analyzed by Ingenuity Pathways Analyses. 256 genes and 18 gene networks were significantly associated with GBS (fold change ≥2, P<0.05). FOS, PTGS2, HMGB2 and MMP9 are the top four of 246 significantly up-regulated genes. The most significant disease and altered biological function genes associated with GBS were those involved in inflammatory response, infectious disease, and respiratory disease. Cell death, cellular development and cellular movement were the top significant molecular and cellular functions involved in GBS. Hematological system development and function, immune cell trafficking and organismal survival were the most significant GBS-associated function in physiological development and system category. Several hub genes, such as MMP9, PTGS2 and CREB1 were identified in the associated gene networks. Canonical pathway analysis showed that GnRH, corticotrophin-releasing hormone and ERK/MAPK signaling were the most significant pathways in the up-regulated gene set in GBS.
  
  
  CONCLUSIONS
  This study reveals the gene networks and canonical pathways associated with GBS. These data provide not only networks between the genes for understanding the pathogenic properties of GBS but also map significant pathways for the future development of novel therapeutic strategies.
authors.affiliation: Department of Neurology, Chang Gung Memorial Hospital Linkou Medical Center and College of Medicine, Chang Gung University, Taiwan, Republic of China.
authors.forename: Kuo-Hsuan
authors.initials: KH
authors.lastname: Chang
authors.forename: Tzi-Jung
authors.initials: TJ
authors.lastname: Chuang
authors.forename: Rong-Kuo
authors.initials: RK
authors.lastname: Lyu
authors.forename: Long-Sun
authors.initials: LS
authors.lastname: Ro
authors.forename: Yih-Ru
authors.initials: YR
authors.lastname: Wu
authors.forename: Hong-Shiu
authors.initials: HS
authors.lastname: Chang
authors.forename: Chin-Chang
authors.initials: CC
authors.lastname: Huang
authors.forename: Hung-Chou
authors.initials: HC
authors.lastname: Kuo
authors.forename: Wen-Chuin
authors.initials: WC
authors.lastname: Hsu
authors.forename: Chun-Che
authors.initials: CC
authors.lastname: Chu
authors.forename: Chiung-Mei
authors.initials: CM
authors.lastname: Chen
mesh_terms: D017318:Annexin A3 / Q000235:genetics / Q000378:metabolism; D016022:Case-Control Studies; D015536:Down-Regulation / Q000235:genetics; D005260:Female; D053263:Gene Regulatory Networks / Q000235:genetics*; D020275:Guillain-Barre Syndrome / Q000201:enzymology / Q000235:genetics*; D006801:Humans; D007962:Leukocytes / Q000378:metabolism; D008297:Male; D020782:Matrix Metalloproteinases / Q000235:genetics / Q000378:metabolism; D008875:Middle Aged; D015203:Reproducibility of Results; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000235:genetics*; D059467:Transcriptome / Q000235:genetics; D015854:Up-Regulation / Q000235:genetics
chemical_list: D017318:Annexin A3; D020782:Matrix Metalloproteinases