RT Journal Article
SR Electronic
T1 Gene expression in peripheral blood mononuclear cells from patients with chronic fatigue syndrome
JF Journal of Clinical Pathology
JO J Clin Pathol
FD BMJ Publishing Group Ltd and Association of Clinical Pathologists
SP 826
OP 832
DO 10.1136/jcp.2005.025718
VO 58
IS 8
A1 N Kaushik
A1 D Fear
A1 S C M Richards
A1 C R McDermott
A1 E F Nuwaysir
A1 P Kellam
A1 T J Harrison
A1 R J Wilkinson
A1 D A J Tyrrell
A1 S T Holgate
A1 J R Kerr
YR 2005
UL http://jcp.bmj.com/content/58/8/826.abstract
AB Background: Chronic fatigue syndrome (CFS) is a multisystem disease, the pathogenesis of which remains undetermined. Aims: To test the hypothesis that there are reproducible abnormalities of gene expression in patients with CFS compared with normal healthy persons. Methods: To gain further insight into the pathogenesis of this disease, gene expression was analysed in peripheral blood mononuclear cells from 25 patients with CFS diagnosed according to the Centers for Disease Control criteria and 25 normal blood donors matched for age, sex, and geographical location, using a single colour microarray representing 9522 human genes. After normalisation, average difference values for each gene were compared between test and control groups using a cutoff fold difference of expression ⩾ 1.5 and a p value of 0.001. Genes showing differential expression were further analysed using Taqman real time polymerase chain reaction (PCR) in fresh samples. Results: Analysis of microarray data revealed differential expression of 35 genes. Real time PCR confirmed differential expression in the same direction as array results for 16 of these genes, 15 of which were upregulated (ABCD4, PRKCL1, MRPL23, CD2BP2, GSN, NTE, POLR2G, PEX16, EIF2B4, EIF4G1, ANAPC11, PDCD2, KHSRP, BRMS1, and GABARAPL1) and one of which was downregulated (IL-10RA). This profile suggests T cell activation and perturbation of neuronal and mitochondrial function. Upregulation of neuropathy target esterase and eukaryotic translation initiation factor 4G1 may suggest links with organophosphate exposure and virus infection, respectively. Conclusion: These results suggest that patients with CFS have reproducible alterations in gene regulation.