Saturday, February 27, 2010

Italian researchers discover a possible onset mechanism for Multiple Sclerosis

I just read an interesting article on how bacterium might be a trigger for the onset of Multiple Sclerosis. One theory regarding the cause of MS is that it is an autoimmune triggered. A recent study in mice found that a harmless bacterium made to look like a nerve cell allows T-cells to modify to the point where they can repeatedly break into the central nervous system. Normally, T-cells can not do this. However, in mice where this modified bacterium has been introduced, the T-cells modify in the inflammatory response. These modified T-cells persist well after the bacterium has been killed and continue to cause inflammation in the central nervous system.

I think it's interesting to see how other immune disorders operate as there may be analogs in Crohn's.

Here's an excerpt:
This is the hypothesis that the researchers coming from the Institutes of General Pathology, Microbiology and Anatomy of the Catholic University of Rome have been testing with their two-year long work. To demonstrate the viability of this idea, scientists have fooled the mouse immune system, modifying subtly a bacterium of the common family of mycobacteria (the same family to which also the bacterium causing tuberculosis belongs) to make it look like to myelin, the protein coating nerve cells. This modified mycobacterium is completely innocuous. As all external agents, though, it is capable to trigger the reaction of the T-cells of the immune systems. They intervene to destroy it. Since they are innocuous bacteria, although very common in the environment, and since they induce an immune reaction, they are the ideal bacteria scientists can use to study the environmental factor contributing, together with the genetic factor, to cause multiple sclerosis.

"Normally, T-cells cannot penetrate into the Central Nervous System", adds Rea, "because the hematoencephalic barrier prevents them from doing so. But the bacterium modifies the characteristics of the T-cells and allows them to overcome the barrier. In 15 days the bacterium disappears completely from the body".

Yet these T-cells can now enter into the brain. This way, they begin to attack the myelin of the nerve cells, and here is how the immune disease breaks out.

"We basically demonstrate – explains Rea – that in an animal model it is possible to be infected with something not carrying any disease, and later on develop a purely autoimmune disease".

Pretty interesting.

Thursday, February 25, 2010

Alberta a 'hot spot' for Crohn's

Saw this article about the high prevalence of Crohn's and Colitis in Alberta and thought it was interesting. They are planning to undertake a large research study there to look for common reasons that could be contributing factors. Looking forward to seeing the results.

Saturday, February 20, 2010

TRPV2 Protein Trips Up Germs

Another article on proteins related to the immune response. TRPV2 allows macrophages to get a better grip on bacteria, allowing the immune response to be more effective. There's no direct relationship found at this point with autoimmune diseases like Crohn's, but you never know. So thought I'd post it.

Here's an excerpt:

Citing the fact that TRPV2 is important not only in helping macrophages to bind to germs, but also in clearing bacterial infection, Caterina noted its potential as a useful drug target. And in cases of autoimmune diseases -- arthritis, lupus and asthma, for example -- it's possible that the inhibition of TRPV2 might help pull back an overactive immune system.

"We think there are going to be a lot of implications beyond just prevention of infectious diseases where this research about TRPV2's function in macrophages might be relevant," Link adds. "Macrophages consume cholesterol and contribute to hardening of the arteries. They also clear out debris when nerves are injured so that new nerves can grow through that area."

GM-CSF Protein Appears Key to Intestinal Balance

Saw this article and thought it was interesting. It's about a protein called granulocyte-macrophage colony-stimulating factor (GM-CSF) that helps regulate gut inflammation.

Here's an excerpt:

Reduced levels of the protein — granulocyte-macrophage colony-stimulating factor (GM-CSF) — could be an underlying factor in severe illness caused by pathogens such as E. coli and intestinal inflammation in inflammatory bowel diseases such asCrohn’s disease, the researchers said.

“The gut normally is in a chronic state of low-grade inflammation that is beneficial,” study author Dr. Martin Kagnoff, professor emeritus of medicine and pediatrics at the University of California, San Diego, School of Medicine, said in a university news release.

“This study shows that GM-CSF has a profound influence in the regulation of cells that determine whether the gut lives in peace with this inflammation or becomes severely inflamed during infection,” he said. “Any time that delicate balance is disrupted, all heck can break loose.”

Kagnoff said the findings might help explain why some people with Crohn’s disease benefit from receiving GM-CSF. A greater understanding of the role of GM-CSF in the gut could lead to new treatments based on the protein, he added.

Saturday, February 6, 2010

Link Between Inflammatory Disease and Premature Aging

Some research from University of Arizona suggests that inflammatory diseases, including inflammatory bowel diseases like Crohn's Disease, could lead to a premature aging process. The researchers found that the Klotho gene, a gene which plays a vital role in aging, was down-regulated. This could speed the onset of age-related diseases like osteoporosis.

Here's one excerpt:
"We have made a novel discovery," said Dr. Fayez K. Ghishan, professor and director of the Steele Center. "Based on our research, it appears that chronic inflammation of the gut causes Klotho to down-regulate – or ‘turn off' – contributing to premature-aging diseases such as osteopenia, osteoporosis and atherosclerosis, to name a few."
And another excerpt:
"We can now theorize that if you have an inflammatory process going on, like IBD or rheumatoid arthritis, for example, you are likely to develop symptoms of premature aging," Kiela said. "Our findings lay the foundation for future work related to the contribution of Klotho to chronic inflammatory diseases in human patients – and how to better treat these diseases."

Distinct demographic profiles between Crohn's disease and ulcerative colitis

Just read a short article on the demographic differences between UC and CD sufferers in the UK. Additional support for environmental differences being a contributing factor. Interesting that CD was more common among "deprived social groups". Perhaps a different diet in that group? Here's an excerpt:

They found that hospitalization for severe CD was more common among women than men and it peaked among younger people aged 16󈞉 years. UC was similar among men and women and was more common among older people. There was no link between social deprivation and UC, but CD was more common among more deprived social groups.

The differing demographic profiles between CD and UC, suggest that environmental factors play a more significant role in the etiology of CD. The findings of this large population-based study on the prevalence and mortality of IBD are also important for service planning and provision.