Confirmatory study of gene expression in peripheral blood of patients with Gulf War Syndrome
Dr Jonathan Kerr
Investigator
Dr Jonathan R Kerr
Institution
St George’s University of London, London, UK
Aims and Methods
Gulf War Syndrome (GWS) is a constellation of symptoms which were reported with a significant incidence in military personnel who fought in the first Gulf War. The most frequent complaints among veterans are fatigue, rashes, joint pains, muscle pains, neuropsychiatric complaints, shortness of breath, sleep disturbances and gastrointestinal problems. Various triggers and mechanisms have been proposed, and it has been shown that the symptoms in veterans with GWS are associated with cellular immune activation though the precise abnormalities remain to be determined and alternative approaches are urgently needed.
There is controversy surrounding this illness, and the situation has clear parallels with Chronic Fatigue Syndrome (CFS). These syndromes exhibit similar symptoms and Gulf War Wyndrome patients often also fulfil the CDC criteria for diagnosis of CFS (Fukuda et al, 1994). In addition, they probably have aetiologic triggers and disease mechanisms in common; for example, both illnesses diseases have a Th2 lymphocyte response. Importantly, both Gulf War Syndrome and ME/CFS exhibit indisputable organic and biological abnormalities, and these must be characterised.
This group has been investigating the molecular pathogenesis of ME/CFS as a collaboration for 5 years. Its goals are to elucidate the disease mechanisms through study of peripheral blood gene expression, to identify protein biomarkers which will facilitate development of a diagnostic test for ME/CFS, and to develop novel treatments which will cure most cases of the disease (Kerr et al, 2006). It has performed a pilot study of gene expression in CFS patients compared with controls (Kaushik et al, 2005) and has demonstrated marked human gene dysregulation, principally affecting the immune system. These findings have been confirmed using a large microarray and real-time PCR (Kerr et al, 2006). It has also performed a pilot study looking for protein biomarkers and has shown several molecules which are specific to ME/CFS and which must now be further characterised towards development of a diagnostic test.
The aim of this confirmatory study (which we are co-funding with the Irish ME Trust) is therefore to elucidate the pathogenesis of Gulf War Syndrome through characterisation of human gene expression and protein analysis in 25 Gulf War Syndrome patients (defined according to Haley criteria) and 25 matched healthy blood donors, and to determine if these mechanisms are similar to those that the group has already identified in ME/CFS. Whatever the outcome, the comparison will be instructive, and will help elucidate the meaning of the genetic ‘signature’ for ME/CFS.
