Lyme disease, science, and society: Camp Other

Tuesday, October 25, 2011

0 Stony Brook Young Investigators Series On Lyme Disease

Ixodus ticks that carry B.burgdorferi.
Photo Credit: http://www.freewebs.com/
lymeandautism/GF-596-4ticks_cm.jpg
Stony Brook University has an online journal of science called The Young Investigators where students from the school write an in-depth article with citations on different topics.

Nadya Peresleni, Editor in Chief of the journal and undergraduate class of 2011, wrote a report on Lyme disease that I think is pretty good - it's detailed, touches upon the controversy over treatment in a matter-of-fact manner, describes the immunological and inflammatory aspects of the infection, and leaves some ideas about areas to target for future treatment options.

I found this paragraph to be of interest, and there is much more in the article that is good to read:
"Along with Dr. Benach's work, the laboratory of Professor Martha B. Furie has published on the role of interferon-gamma (IFN-γ), a cell-signaling molecule of the immune system, in the endothelial tissue of a genetically engineered mouse model that was infected with B. burgdorferi. 
"IFN-γ is like a molecular switch that turns on chronic inflammation," explained Dr. Furie. When the bacteria disseminate throughout the body after the tick bite, they activate the endothelium and begin the inflammatory process by attracting T lymphocytes that secrete IFN-γ [22]. The inflammation was found to be due, in large part, to a synergistic effect of B. burgdorferi and IFN-γ, which together activate the transcription of a series of genes in endothelial cells. These genes encode chemokines, or chemoattractants, specific for T lymphocytes. 
Interestingly, there seemed to be selection for those T lymphocytes that secreted more IFN-γ, and the result was a positive feedback loop that generated more and more IFN-γ, leading to a state of chronic inflammation in the tissue. The damage to human tissues is likely caused by the body's reaction to the bacteria, not the bacteria themselves [22]."

Yes, but the question remains as to whether the damage left behind is causing symptoms - or if the inflammation is caused by bacteria which are still viable is part of the problem... Or both.

This article mentions persistent infection and offers citations to examples - and it also mentions the above kind of mechanism for producing symptoms.

Check out the entire article here: http://www.younginvestigators.com/article-lyme-disease-overview.php


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