The articles from this week discussed the important role of interleukin-10 in post ischemic stroke. We understood that the lack of IL-10 could result in further brain injury from excess inflammation caused by unregulated cytokines secretions, as well as less chance of recovery (no significant reduction of infarction size or progressed physical movements and verbal ability).
One of the articles raised a question about why stroke patients exhibit a different anti-inflammatory profile. It mentioned briefly about the interleukin-10 gene polymorphism and therefore I did some further research on this issue.
Various studies have shown the correlation between IL-10 polymorphism and a higher risk of death or lower ability to deal with infections and diseases.
The particular study I read was in the case of sudden infant death syndrome (SIDS) where the studies found a difference in the percentage of genotypes between the control and experiment groups. The study discovered higher percentage genotype G21/G22 of the SIDS patients than in the controls. The individuals with an unfavorable IL-10 genotype exhibited abnormal IL-10 production which leads to imbalanced immune response upon infection.
My question towards these various studies is - if IL-10 gene polymorphism is known to be the main reason causing lower secretion of IL-10, perhaps many diseases or deaths (including stroke) could be prevented? A few research articles I read that are related to IL-10 gene polymorphism were pulmonary diseases, Hodgkin's Lymphoma, SIDS, etc. However, I have not yet read about any methods or technology to perform on newborns for diagnosing such deficit of genes.
Opdal SH, Opstad A, Vege A, Rognum TO
IL-10 gene polymorphisms are associated with infectious cause of sudden infant death.
Institute of Forensic Medicine, University of Oslo, Rikshospitalet University Hospital, 0027 Oslo, Norway.
Human Immunology. 2003 Dec;64(12):1183-9
Subscribe to:
Post Comments (Atom)
It seems as if these studies point to the fact that lowered production of an anti-inflammatory cytokine such as IL-10 results in the body's decreased ability to prevent damaging inflammation. While that knowledge is all well and good, it is more difficult to determine the best therapeutic approach that utilizes the knowledge. The seemingly simple manner would be to add more IL-10 to the body (as the SNP downregulates IL-10 production), however, formulating protein therapeutics is a very tricky business, as proteins balance precariously on an edge between instability and too stable. Furthermore, it may be too late to start therapy once the disease presents itself-the damage may already be done. Does that mean all newborns should be genetically tested for the IL-10 SNP so that preventitive treatment can be started? What if, when adding IL-10 into the body, you add too much, and over-regulate the body's natural inflammatory response?
ReplyDelete