Hashimoto’s thyroiditis: modern views on the pathogenesis (literature review)

• Main Authors: V.А. Shidlovskyi, А.V. Shidlovskyi, M.I. Sheremet, L.P. Sydorchuk, I.V. Pankiv
• Format: Article
• Language: English
• Published: Publishing House Zaslavsky 2020-05-01
• Series: Mìžnarodnij Endokrinologìčnij Žurnal
• Subjects: hashimoto’s thyroiditis; pathogenesis; intestinal dysbacteriosis; immune system; review
• Online Access: http://iej.zaslavsky.com.ua/article/view/208489

There is a steady increase in the incidence of Hashimoto’s autoimmune thyroiditis worldwide. The etiology and pathogenetic mechanisms of its development are unknown. It is believed that the cause may be increasing and rapidly changing antigenic load on the immune system by environmental triggers such as the nature and quality of food, intestinal dysbacteriosis, bacterial, viral and fungal infections. Due to the action of several of these factors or one of them, the intestinal immune system loses the ability to identify antigens that come with food and mistakenly begins to produce antibodies to body tissues. Leading importance in the development of this process is given to intestinal dysbacteriosis. The review analyzes the literature data on the importance of dysbacteriosis and the intestinal immune system in the deve­lopment of autoimmunity and Hashimoto’s thyroiditis. The natural intestinal microflora is in close and constant contact with the immune system of the mucous membrane. The immune system limits the invasion of intestinal wall tissues by a wide variety of microbes, including potential pathogens that can be ingested with food. Despite immune barriers, bacteria can find ways to cross the epithelial layer. In this case, the mechanisms of bacterial destruction are triggered — phagocytosis and elimination by macrophages. Intestinal dysbacteriosis leads to autoimmune diseases and changes the usual modes of digestion and absorption, the functioning of the mucous membrane and the immune system. Intestinal dysbacteriosis causes a violation of the functional density of its mucous membrane. The essence of this process is that the amount of protein that fills the space between the enterocytes and binds them together, thus forming a protective barrier, is reduced in dysbacteriosis. This process is regulated by a specific protein zonulin, which under physiological conditions regulates the absorption of food ingredients and creates a selective permeability of molecules. In dysbacteriosis, the selective permeability of the intestinal wall is lost. Toxins, products of incomplete hydrolysis and other antigens that create a load on the immune system begin to pass through it. These processes lead to food intolerance, allergies and the deve­lopment of autoimmunity.