You did this! ‘Crowdsourcing raises vital funds for ME research’ – http://t.co/V3XEfT9AIF did you spot Prof LDIfME? pic.twitter.com/z7gXszm0Tk      

— Let’s Do It for ME! (@LetsDoIt4ME) March 31, 2014

Autoimmune reactions lead to inflammation, increased permeability of blood vessels and migration of lymphocytes to sites of injury. Microglia within the brain can be primed during chronic inflammatory diseases, but can then induce inflammation in the brain when they are triggered by a second inflammatory challenge such as a systemic microbial infection. This raises the possibility that the damaging neuro-inflammation seen during ME may be triggered by systemic infections.

The gastrointestinal tract contains a microbiota consisting of a vast number of bacteria and viruses. The microbiota can influence intestinal barrier function and host defence against microbial challenge. Changes in the microbiota can cause local and systemic chronic inflammation. This project will determine if alterations in intestinal barrier function and/or microbiota exist in ME patients, and whether microbe-driven inflammatory responses can provide an explanation for the pathophysiology of ME.

• The project began in October 2013.

• The cohort selected fit the Canadian Consensus Criteria and include the severely affected.

• The studentship is based in the Norwich Medical School and Quadram Insitute Bioscience.

• The student will analyse serum samples from patients with ME for integrity of intestinal barrier function.

• Faecal samples from patients will be analysed by high throughput pyrosequencing and appropriate bioinformatics to profile the microbiota in terms of bacteria and virus populations.

• Parallel studies will assess microbiota metabolism by LC/MS/NMR analysis by the IFR Metabolomics Partnership.

  For full details click here

‘Defining autoimmune aspects of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome‘

The aim of this PhD project is to test the hypothesis that ME is an autoimmune disorder originating in the gut as a consequence of altered intestinal permeability (leaky gut) leading to exposure of the immune system to commensal gut microbes and their products and the generation of pathogenic (auto) antibodies cross-reactive with antigens expressed in the central nervous system (CNS).

For full details click here

‘Gut Viruses and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome‘

This PhD project will investigate whether the underlying causes of ME are related to the presence of specific virus populations within the gut virobiota. Using high throughput DNA/RNA sequencing technology and bioinformatics tools we will determine if and how both resident gut bacteria and virus populations changes with disease progression and if a distinct virobiota signature can be identified in ME patients.

For full details click here

‘Investigating alterations in the intestinal virome in ME‘

This PhD project will investigate and aim to answer important questions concerning the role of the enteric phage/virome in ME. Specifically, can long-read sequencing identify new enteric phages, many of which may have been locked within the ‘viral dark matter’? Do the phages populations differ between patients and controls? Can the phages identified reduce populations of ‘beneficial bacteria’ and/or affect the metabolism of the microbiota? Can phage DNA profiling be used in biomarker development for ME?

For full details click here

‘Extended B cell phenotype in patients with myalgic encephalomyelitis/chronic fatigue syndrome: a cross‐sectional study‘

A preliminary B-cell study was designed to confirm and extend the earlier work of Dr. Amolak Bansal [1] on B-cells but using a different cohort of ME patients. This was advised as prerequisite to a UK trial of rituximab but also a useful study in its own right. The study was published in the official Journal of the British Society of Immunology, Clinical and Experimental Immunology.

For full details click here.

‘The potential role of B cells and their products in ME/CFS Patients‘

Recent studies have identified abnormalities in the blood of patients, which have strengthened the suspicion that the immune system contributes to ME/CFS. Changes in populations of white blood cells, called B cells, in ME/CFS have been reported by several research groups including those in the UK. In addition, treatment with anti-B cell therapy using Rituximab by Fluge and colleagues in Norway have shown benefit to ME patients. This PhD project will investigate whether certain B cell products (antibodies and soluble factors) are involved in ME/CFS.

For full details click here.