The role of IgG hypersensitivity in the pathogenesis and therapy of depressive disorders.

Depressive episodes are associated not only with changes in neurotransmission in the central nervous system, but also may lead to structural changes in the brain through neuroendocrine, inflammatory, and immunological mechanisms. The aim of this article is to present a new hypothesis connecting the inflammatory theory of depression with IgG food hypersensitivity and leaky gut syndrome. This new potential pathway that may mediate the pathogenesis of depression implies the existence of subsequent developmental stages. Overproduction of zonulin triggered, for example, by gliadin through activation of the epidermal growth factor receptor and protease-activated receptor causes loosening of the tight junction barrier and an increase in permeability of the gut wall ('leaky gut'). This results in a process allowing larger molecules that would normally stay in the gut to cross into the bloodstream and in the induction of IgG-dependent food sensitivity. This condition causes an increased immune response and consequently induces the release of proinflammatory cytokines, which in turn may lead to the development of depressive symptoms. It seems advisable to assess the intestinal permeability using as a marker, for example, zonulin and specific IgG concentrations against selected nutritional components in patients with depression. In the case of increased IgG concentrations, the implementation of an elimination-rotation diet may prove to be an effective method of reducing inflammation. This new paradigm in the pathogenesis of depressive disorders linking leaky gut, IgG-dependent food sensitivity, inflammation, and depression is promising, but still needs further studies to confirm this theory.

Interleukin 17 receptor in multiple sclerosis patients treated with interferon ß-1a.

Interleukin 17 (IL-17) and its receptor IL-17R1 produced by T-helper cells named Th17 are involved in the pathology of autoimmune diseases. In contrast to the at least partially explained role of IL-17 in pathology of multiple sclerosis, the significance of IL-17R in MS is unclear. Therefore we have studied the expression of IL-17R in the stable phase of multiple sclerosis treated by interferon ß-1a. The studied material consisted of 20 MS patients with relapsing-remitting form of the disease, and fulfilling the diagnostic McDonald et al. criteria. The patients were treated subcutaneously every second day with 30 mg of interferon ß -1a (Betaferon). The interleukin 17 receptor level was measured by the ELISA immunoassay test using RayBio human IL-17R ELISA kit. After three months of therapy with interferon ß -1a the level of IL-17R was significantly higher than that established at the starting point. The level of IL-17R after 6 months of therapy was insignificantly higher than established in the previous study group (3 months of therapy). While it remains difficult to pinpoint the exact significance of upregulation of IL-17R in the early period of therapy, the present findings should be taken into account when considering the pharmacodynamics of interferon action in MS in view of the opinions on the crucial role of IL-17 in pathology of MS and suggestions that it may constitute a drug target in autoimmunological diseases.