This recent review is from the Brazilian journal  Arq. Bras. Oftalmol. 2012 Apr; vol. 75(2) pp. 143-7  For those with a scientific/medical background, the whole of paper can be found at the following link.   http://www.scielo.br/scielo.php?pid=0004-2749&script=sci_issues

The review, written by medics, ophthalmologists and students, describes the main experimental models of autoimmune ocular inflammatory diseases.  The hope is that by better understanding the process of autoimmune ocular inflammation in animal models, it will lead to a better understanding of human ocular inflammation.

The paper concludes that the current and new models experimental models being developed may help us to develop new therapies with fewer side effects or new ways of delivering therapies.

Exciting news – there seems to be so much work going on around autoimmune posterior uveitis.  For those of you who want a fuller read, we reproduce the conclusion of the review below:

CONCLUSION

“Researches on experimental models have been important to explain the pathophysiological mechanisms involved in different ocular autoimmune inflammatory diseases. EAU is one of the most used animal models. After immunization with uveitogenic antigens, animals develop an immune response mediated primarily by CD4+ T cells. Clinical findings are somewhat similar to some human autoimmune uveitis. Even though these models contribute for a better understanding of the pathophysiology of autoimmune uveitis in humans, there are still many questions to be answered, such as triggers, recurrences, and individual susceptibility. Heterogeneous clinical findings may be related to the observation that each subject may respond to more than one epitope per antigen and respond differently to each one of them, depending on how it is presented and how it is recognized by the immune system.

Lately, new ocular inflammatory experimental models have been available due to the advances in genetics and molecular engineering. These models may help the development of news therapies, with more specific and efficient drugs, avoiding side effects. In addition, animal models are important for the study of new routes of drug delivery, especially by intravitreal injection.

Many of us believe that stress may be a contributory factor in our Birdshot and in flare-ups.  Stress has been linked to auto-immune diseases and it is commonly thought that there is a stress relationship with flare-ups in other forms of Uveitis.

A paper by R Khanfer , G Wallace, P A Keane, and A C Phillips has reviewed what is currently known about the relationship between uveitis and psychological stress.

Birdshot Uveitis Society knows two of the authors well.  Dr Graham Wallace was one of the speakers at our last Birdshot Day,  and Pearse Keane, whilst unable to attend the Day, has been a key professional working in the field of Birdshot, and will be attending our next Day.   Pearse was introduced to us by BUS member Nick Bucknall and consultant Alastair Denniston.  Both Pearse and Alastair are very interested in  OCT imaging in relation to Birdshot Uveitis and have been working on research in this field as well.

Here is an abstract from the paper:

“Uveitis is an inflammatory condition affecting the eye and is often associated with systemic autoimmune disease. A role for the involvement of psychological stress in autoimmune disease has been widely demonstrated. However, uveitis is not classified as an autoimmune disease, and a definite or direct cause has yet to be identified, although infection may be involved. Many uveitis patients retrospectively report stressful life events occurring prior to the onset or recurrence of uveitis. However, only a small number of studies have explored the potential association between psychological stress and uveitis, and their findings are somewhat contradictory, many showing that the experience of uveitis itself results in stress. ”

It is really interesting to see this piece of research, and our own quality of life survey should help to begin to answer some of the questions:  Is it stress that helps trigger Birdshot (or the severity of Birdshot) or Birdshot that triggers stress or medication that leads to stress and causes flare ups?

Read the full article at the link below.

PMID: 22685876

URL – http://www.ncbi.nlm.nih.gov/pubmed/22685876?dopt=Citation

We have recently posted about the importance of ensuring that we get the right diagnosis, testing and monitoring for Birdshot as other diseases can often look like Birdshot, but will require totally different treatments.  A research paper from the Massachusetts Eye and Ear infirmary in Boston has recently been published, and builds on this theme.

The paper examines ways in which to test and monitor for Birdshot, and is really useful in helping us understand the monitoring tests we get, and why we get them.

In short, the paper explains that it is critical to diagnose and carefully monitor Birdshot as it can progress insidiuously without any associated pain, and looking just for visual acuity, inflammation or vascular leakage of fluorescein alone, may not be effective.

The authors of the paper review the current methods of diagnosing, testing and monitoring for Birdshot including ERGs, fluorescine angiography, indocyanine green angiography, OCTs, visual field tests and HLA A29 blood testing.

The major finding is that 70% of people with Birdshot have abnormal readings on one of the parameters (the 30 hz flicker) of ERGs.  This is really interesting, as it means that ERGs may be a fairly good way to help diagnose Birdshot.  It also could mean that if we have a ‘normal’ 30 hz flicker result, we may be able to reduce our medication.

This does not mean, of course, that we can do without some of the other monitoring – each system has its uses.  For example, OCT is particularly pertinent if you have macular oedema, and we posted recently about the importance of indocyanine green angiography.  However, it does help us, as patients with Birdshot, understand why all these tests are so very important in ensuring that we maintain our visual acuity and are not under or over medicated, and that our medication regimes are effective.

Read the full article by clicking the link below.

AUTHORS: Comander J, Loewenstein J, Sobrin L

PMID: 21958183

URL – http://www.ncbi.nlm.nih.gov/pubmed/21958183?dopt=Citation

An interesting piece of research has just been reported on.  The research, undertaken by a team, led by Dr Suzanne Hodgkinson from the University of New South Wales in Australia has found that injecting interleukin-5 into rats with Guillain-Barre syndrome (an autoimmune disease) makes them recover much more quickly, and if given as a preventative measure, ensured they did not fall ill.  It seems that this treatment may also be effective in other autoimmune conditions (Birdshot is an autoimmune disease – perhaps it will work for us?).

The exciting thing about this kind of treatment is that it works by increasing the amount of ‘good’ cells.  Much of our current treatment relies on trying to suppress our ‘bad’ cells.

Even more interestingly, you may remember that we posted about a promising (although rather off-putting) treatment called helminthic therapy.  This therapy involves worms which change your immune response and helminthic therapy is currently being trialled on several different kinds of autoimmune diseases.  When you have an helminthic infestation, your immune system responds by increasing the production of eosinophils which make the cytokine interleukin-5.

Dr Suzanne Hodgkinson says ‘ In this new treatment, it’s a matter of injecting the interleukin-5 and the body does the rest.  It’s both safe and effective and we think inducing the immune response by injection may be more attractive to people than swallowing parasitic worms’.

We say, please hurry up and start trialling this on us Birdshotters!  Anything to avoid worms!!

Read the full article at

http://bloodjournal.hematologylibrary.org/content/119/19/4441.abstract