BACKGROUND: Intestinal inflammation is a common feature of spondyloarthropathy (SpA) and Crohn's disease. Inflammation is manifested clinically in Crohn's disease and subclinically in SpA. However, a fraction of patients with SpA develops overt Crohn's disease. AIMS: To investigate whether subclinical gut lesions in patients with SpA are associated with transcriptome changes comparable to those seen in Crohn's disease and to examine global gene expression in non-inflamed colon biopsy specimens and screen patients for differentially expressed genes. METHODS: Macroarray analysis was used as an initial genomewide screen for selecting a comprehensive set of genes relevant to Crohn's disease and SpA. This led to the identification of 2625 expressed sequence tags that are differentially expressed in the colon of patients with Crohn's disease or SpA. These clones, with appropriate controls (6779 in total), were used to construct a glass-based microarray, which was then used to analyse colon biopsy specimens from 15 patients with SpA, 11 patients with Crohn's disease and 10 controls. RESULTS: 95 genes were identified as differentially expressed in patients with SpA having a history of subclinical chronic gut inflammation and also in patients with Crohn's disease. Principal component analysis of this filtered set of genes successfully distinguished colon biopsy specimens from the three groups studied. Patients with SpA having subclinical chronic gut inflammation cluster together and are more related to those with Crohn's disease. CONCLUSION: The transcriptome in the intestine of patients with SpA differs from that of controls. Moreover, these gene changes are comparable to those seen in patients with Crohn's disease, confirming initial clinical observations. On the basis of these findings, new (genetic) markers for detection of early Crohn's disease in patients with SpA can be considered.
BACKGROUND: Intestinal inflammation is a common feature of spondyloarthropathy (SpA) and Crohn's disease. Inflammation is manifested clinically in Crohn's disease and subclinically in SpA. However, a fraction of patients with SpA develops overt Crohn's disease. AIMS: To investigate whether subclinical gut lesions in patients with SpA are associated with transcriptome changes comparable to those seen in Crohn's disease and to examine global gene expression in non-inflamed colon biopsy specimens and screen patients for differentially expressed genes. METHODS: Macroarray analysis was used as an initial genomewide screen for selecting a comprehensive set of genes relevant to Crohn's disease and SpA. This led to the identification of 2625 expressed sequence tags that are differentially expressed in the colon of patients with Crohn's disease or SpA. These clones, with appropriate controls (6779 in total), were used to construct a glass-based microarray, which was then used to analyse colon biopsy specimens from 15 patients with SpA, 11 patients with Crohn's disease and 10 controls. RESULTS: 95 genes were identified as differentially expressed in patients with SpA having a history of subclinical chronic gut inflammation and also in patients with Crohn's disease. Principal component analysis of this filtered set of genes successfully distinguished colon biopsy specimens from the three groups studied. Patients with SpA having subclinical chronic gut inflammation cluster together and are more related to those with Crohn's disease. CONCLUSION: The transcriptome in the intestine of patients with SpA differs from that of controls. Moreover, these gene changes are comparable to those seen in patients with Crohn's disease, confirming initial clinical observations. On the basis of these findings, new (genetic) markers for detection of early Crohn's disease in patients with SpA can be considered.
Authors: P Demetter; D Baeten; F De Keyser; M De Vos; N Van Damme; G Verbruggen; S Vermeulen; M Mareel; D Elewaut; H Mielants; E M Veys; C A Cuvelier Journal: Ann Rheum Dis Date: 2000-03 Impact factor: 19.103
Authors: J D Rioux; M S Silverberg; M J Daly; A H Steinhart; R S McLeod; A M Griffiths; T Green; T S Brettin; V Stone; S B Bull; A Bitton; C N Williams; G R Greenberg; Z Cohen; E S Lander; T J Hudson; K A Siminovitch Journal: Am J Hum Genet Date: 2000-04-21 Impact factor: 11.025
Authors: J H Cho; D L Nicolae; R Ramos; C T Fields; K Rabenau; S Corradino; S R Brant; R Espinosa; M LeBeau; S B Hanauer; J Bodzin; D K Bonen Journal: Hum Mol Genet Date: 2000-05-22 Impact factor: 6.150
Authors: Dominique Baeten; Pieter Demetter; Claude A Cuvelier; Elli Kruithof; Nancy Van Damme; Martine De Vos; Eric M Veys; Filip De Keyser Journal: J Pathol Date: 2002-03 Impact factor: 7.996
Authors: M Dougados; S van der Linden; R Juhlin; B Huitfeldt; B Amor; A Calin; A Cats; B Dijkmans; I Olivieri; G Pasero Journal: Arthritis Rheum Date: 1991-10
Authors: Christine M Costello; Nancy Mah; Robert Häsler; Philip Rosenstiel; Georg H Waetzig; Andreas Hahn; Tim Lu; Yesim Gurbuz; Susanna Nikolaus; Mario Albrecht; Jochen Hampe; Ralph Lucius; Günther Klöppel; Holger Eickhoff; Hans Lehrach; Thomas Lengauer; Stefan Schreiber Journal: PLoS Med Date: 2005-08-23 Impact factor: 11.069
Authors: Fernando M Pimentel-Santos; Dário Ligeiro; Mafalda Matos; Ana F Mourão; José Costa; Helena Santos; Anabela Barcelos; Fátima Godinho; Patricia Pinto; Margarida Cruz; João E Fonseca; Henrique Guedes-Pinto; Jaime C Branco; Matthew A Brown; Gethin P Thomas Journal: Arthritis Res Ther Date: 2011-04-07 Impact factor: 5.156
Authors: Anders J Svendsen; Kristina Gervin; Robert Lyle; Lene Christiansen; Kirsten Kyvik; Peter Junker; Christian Nielsen; Gunnar Houen; Qihua Tan Journal: Front Immunol Date: 2016-11-17 Impact factor: 7.561
Authors: Liesbeth Allais; Smitha Kumar; Karlijn Debusschere; Stephanie Verschuere; Tania Maes; Rebecca De Smet; Griet Conickx; Martine De Vos; Debby Laukens; Guy F Joos; Guy G Brusselle; Dirk Elewaut; Claude A Cuvelier; Ken R Bracke Journal: PLoS One Date: 2015-11-02 Impact factor: 3.240