title: [Comparison of the transcriptional profiles of patients with dengue fever and dengue hemorrhagic fever reveals differences in the immune response and clues in immunopathogenesis].
abstract: BACKGROUND
  Dengue infection demonstrates a wide spectrum of clinical manifestations from mild disease (dengue fever) to severe dengue hemorrhagic fever, but the immunopathogenic mechanisms involved in disease severity are not clear.
  
  
  OBJECTIVE
  Differentially expressed genes associated to immune response were identified from peripheral blood mononuclear cells of Colombian children with dengue fever and dengue hemorrhagic fever.
  
  
  METHODS
  Microarray analysis was used as a tool to establish and compare transcriptional profiles of peripheral blood mononuclear cells of six children in acute phase of dengue fever and dengue hemorrhagic fever. The commercial gene chip used was Affymnetrix GeneChip HG_U133_Plus_2.
  
  
  RESULTS
  Dengue hemorrhagic fever patients expressed interleukin 6, chemokines, complement proteins and pentraxin 3, along with the lymphocyte inhibitors lymphocyte-activation gene 3 and cathepsin L1. An interaction model for these genes showed tissue factor playing a central role in the network generated. In contrast, dengue fever patients expressed cytokines, complement and the leukotrienes inhibitors lactotransferrin, C1 inhibitor, and leukotriene-B (4-omega-hydroxylase 2).
  
  
  CONCLUSIONS
  These results indicate that in dengue fever, cytokine and complement inhibitors are able to limit endothelial damage and prevent increases in vascular permeability, whereas dengue- hemorrhagic fever patients have immune cell dysfunction and unregulated complement and cytokine action. This leads to "hypercoagulation" and endothelial damage, thereby increasing disease severity. Verification of the pathogenic role of the identified molecules will contribute to understanding of dengue pathogenesis and lead to rational development of therapeutic drugs.
authors.affiliation: Grupo de Virología, Universidad El Bosque, Bogotá, D.C., Colombia.
authors.forename: Natalia
authors.initials: N
authors.lastname: Houghton-Triviño
authors.forename: Katherine
authors.initials: K
authors.lastname: Martín
authors.forename: Kris
authors.initials: K
authors.lastname: Giaya
authors.forename: Jairo A
authors.initials: JA
authors.lastname: Rodríguez
authors.forename: Irene
authors.initials: I
authors.lastname: Bosch
authors.forename: Jaime E
authors.initials: JE
authors.lastname: Castellanos
mesh_terms: D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D003715:Dengue / Q000235:genetics* / Q000276:immunology* / Q000503:physiopathology; D005260:Female; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000276:immunology*; D053263:Gene Regulatory Networks; D006801:Humans; D007107:Immune System / Q000276:immunology; D007223:Infant; D008297:Male; D046228:Microarray Analysis; D019595:Severe Dengue / Q000235:genetics* / Q000276:immunology* / Q000503:physiopathology; D014158:Transcription, Genetic