One of my short unscheduled 'add-in' posts this one, on what is a bumper crop of papers recently published, or appearing on the research indexes, on coeliac (celiac) disease (CD) and a few related concepts covered on this blog.
The August 2011 issue of the journal, International Reviews of Immunology is a special issue dedicated to all things coeliac disease. The editorial summary can be viewed here. A few papers caught my eye which interested readers might want to follow-up further. This paper on animal models (sorry!) of CD is an interesting one given its summary of the various types of animal model being created to characterise strands of the disease pathology present in CD. The primary conclusion from the work done so far is the leaning towards independent areas of innate, adaptive and auto-immunity all coming together to make CD what it is. This paper connecting CD to intestinal microflora is about as up-to-date as you can get (at least at the time of writing this post) on how our bacterial masters might be tied into CD.
A few other papers on CD to mention also. This paper published in the Journal of Reproductive Medicine highlights an interesting association between problems of female infertility and positive serology for CD. The authors report CD in approximately 6% of their study group presenting with unexplained fertility problems. Perhaps some implications for CD screening? This also follows similar work reporting an association between CD and reproductive life disorders. Although not specifically related to this area, I am reminded of a recent post on risk of CD and your method of entry into the world.
Finally, this paper published in the journal Cellular & Molecular Immunology makes some very interesting observations about the connection between CD and other autoimmune conditions, in this case, type-1 diabetes (T1D). Their findings suggested that where CD and T1D were comorbid in participating children, markers indicated greater intestinal permeability and a 'stronger' immunological response to be present when compared with asymptomatic and mono-CD controls. It seems that an increased autoimmune load might have some cumulative effects, or should that be the other way around?