A healthy intestinal microbiota not only has beneficial effects on the activity of the immune system, but also on thyroid function. The microbiome affects the proper functioning of the thyroid gland, and the existence of the gut-thyroid axis is discussed in the context of both thyroid diseases and gut dysbiosis.
Thyroid and intestinal diseases predominantly coexist: Hashimoto's thyroiditis (HT) and Graves' disease (GD) are the most common autoimmune thyroid diseases (AITD) and often coexist with celiac disease (CD) and non-celiac wheat sensitivity (NCWS). This may be explained by damage to the intestinal barrier and consequent increase in intestinal permeability, allowing antigens to pass more easily and activate the immune system or cross-react with extraintestinal tissues, respectively. Dysbiosis has not only been found in AITD.
The intestine is a target organ of thyroid hormone (TH) that exerts its action through the nuclear receptor for thyroid hormone α1 (TRα1) expressed on intestinal epithelial cells. Disruption of intestinal microbial homeostasis (dysbiosis) is associated with autoimmune thyroid disease (AITD), including Hashimoto's thyroiditis, Graves' disease, and Graves' orbitopathy
The gut microbiota largely regulates the homeostasis and development of immune cells. It modulates both the innate and adaptive immune systems, including outside the intestine, and is essential in the development of gut-associated lymphatic tissue (GALT), where more than 70% of the entire immune system is located. . GALT plays an important role in the development of tolerance to autoantigens by controlling its toll-like receptors (TLRs) in the intestinal mucosa.
There is a positive correlation between the concentration of short-chain fatty acid butyrate and the number of regulatory T cells (TREG), which are key mediators of immune tolerance, as well as with lower concentrations of proinflammatory Th-17 cells. SCFAs can strengthen intercellular tight junctions along with thyroid hormones. The immune system itself influences the composition of the gastrointestinal microbiota, underscoring the symbiotic relationship.
Probiotics have shown beneficial effects in thyroid diseases and may have a positive effect on trace elements such as selenium, zinc and copper. Additionally, microbes function as a reservoir for T3 and can prevent thyroid hormone fluctuation and therefore may reduce the need for T4 supplementation.
The importance of maintaining the intestinal microbiota in a normal state arises from the fact that with increased permeability of the intestine due to dysbiosis, lipopolysaccharides from gram-negative bacteria can enter the bloodstream and contribute to the destruction of the thyroid gland. It has also been shown that SIBO (small intestinal bacterial overgrowth) is seen more frequently in autoimmune hypothyroidism. There is also a potential role for host-microbiota interference in thyroid cancer.
A healthy intestinal microbiota not only has beneficial effects on the activity of the immune system, but also on thyroid function. The microbiome affects the proper functioning of the thyroid gland, and the existence of the gut-thyroid axis is discussed in the context of both thyroid diseases and gut dysbiosis.
Thyroid and intestinal diseases predominantly coexist: Hashimoto's thyroiditis (HT) and Graves' disease (GD) are the most common autoimmune thyroid diseases (AITD) and often coexist with celiac disease (CD) and non-celiac wheat sensitivity (NCWS). This may be explained by damage to the intestinal barrier and consequent increase in intestinal permeability, allowing antigens to pass more easily and activate the immune system or cross-react with extraintestinal tissues, respectively. Dysbiosis has not only been found in AITD.
The intestine is a target organ of thyroid hormone (TH) that exerts its action through the nuclear receptor for thyroid hormone α1 (TRα1) expressed on intestinal epithelial cells. Disruption of intestinal microbial homeostasis (dysbiosis) is associated with autoimmune thyroid disease (AITD), including Hashimoto's thyroiditis, Graves' disease, and Graves' orbitopathy
The gut microbiota largely regulates the homeostasis and development of immune cells. It modulates both the innate and adaptive immune systems, including outside the intestine, and is essential in the development of gut-associated lymphatic tissue (GALT), where more than 70% of the entire immune system is located. . GALT plays an important role in the development of tolerance to autoantigens by controlling its toll-like receptors (TLRs) in the intestinal mucosa.
There is a positive correlation between the concentration of short-chain fatty acid butyrate and the number of regulatory T cells (TREG), which are key mediators of immune tolerance, as well as with lower concentrations of proinflammatory Th-17 cells. SCFAs can strengthen intercellular tight junctions along with thyroid hormones. The immune system itself influences the composition of the gastrointestinal microbiota, underscoring the symbiotic relationship.
Probiotics have shown beneficial effects in thyroid diseases and may have a positive effect on trace elements such as selenium, zinc and copper. Additionally, microbes function as a reservoir for T3 and can prevent thyroid hormone fluctuation and therefore may reduce the need for T4 supplementation.
The importance of maintaining the intestinal microbiota in a normal state arises from the fact that with increased permeability of the intestine due to dysbiosis, lipopolysaccharides from gram-negative bacteria can enter the bloodstream and contribute to the destruction of the thyroid gland. It has also been shown that SIBO (small intestinal bacterial overgrowth) is seen more frequently in autoimmune hypothyroidism. There is also a potential role for host-microbiota interference in thyroid cancer.
https://www.mdpi.com/2072-6643/12/6/1769 (2020).---
https://www.mdpi.com/2077-0383/10/16/3609 (2021).---
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2023.977587/full (2023).---
https://core.ac.uk/download/pdf/580113119.pdf#page=24 (2023).--
https://sirpublishers.org/index.php/jams/article/view/548 (2024).--
https://academic.oup.com/endo/article-abstract/165/1/bqad184/7458951?login=false (2024).---
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