Multiple elements contribute to the origins of autoimmune thyroid disease (AITD). The classical paradigm of autoimmune pathogenesis involving a specific genetic makeup and exposure to environmental triggers has been challenged by the addition of a third element: the loss of intestinal barrier function.
Among these multiple elements, bacteria play a role in the loss of the intestinal barrier function in addition to contributing to the conditions necessary to create a cytokine storm for the onset of autoimmune conditions. For instance, Yersinia enterocolitica seems to be involved in the pathogenesis of Graves’ disease (GD), probably through a mechanism of molecular mimicry between bacterial antigens and thyroid constituents.
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Various studies have shown some link between Helicobacter pylori infection and Autoimmune Thyroid Disease. H. pylori infection does not directly cause Autoimmune Thyroid Disease but has a role in bringing on the autoimmune processes against thyroid.
H. pylori are a stomach bacteria that resides in the mucosal lining of the gastrointestinal tract is responsible for gut inflammation, gastric and duodenal ulcers, gastric mucosa-associated lymphoid tissue lymphoma, and gastric cancer. An H. pylori infection can induce autoimmune processes against the gastrointestinal mucosal lining, with consequent autoimmune gastritis. H. pylori infection are also involved in non-gastrointestinal conditions such as rosacea, heart disease, hair loss, and type 1 diabetes.
H. pylori are one of the most common chronic infections worldwide. It affects approximately 50% of the world population. The majority of those infected never develop clinical symptoms. H. pylori specifically colonize the stomach lining and causes chronic inflammation in the upper digestive tract.
It is well documentedthat gastric mucosa is the main target of H. pylori, which colonizes and damages surface lining and induces a chronic inflammatory response in the mucus lining of the stomach, small intestine and gallbladder. There are many long term consequences of this infection. H. pylori cause damage to glands that produce digestive chemistry and the thickening of the mucus lining reducing the ability to absorb nutrients.
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H. pylori have the ability to shift stomach pH to their preferred alkaline pH. When the preferred alkaline pH is reached, H. pylori produce Lewis antibodies which make them invisible to the immune system while the damage is still occurring. This causes blood and saliva antibody tests for H. pylori to report false negative results. The only test the H. pylori cannot hide from is the Metametrix Gastrointestinal Function Profile (GFP). The GFP is a DNA test similar to those used in court to determine the identities of criminals.
The damage caused by the H. pylori elicits antibodies that cross-react with the components of the gastric mucosal lining, especially parietal cells that secrete gastric acid and intrinsic factor.
This causes the development of adhesions restricting the movement of the stomach and Autoimmune Atrophic Gastritis (AIAG). In fact, a decrease of thyroid antibodies has been observed in patients with AITD even after eradication of H. pylori infection.
The lack of stomach acid or achlorhydria with thickening of the stomach lining also results in the development of anemia as intrinsic factor and B12 metabolism starts failing.
The increased frequency of chronic anemia in patients with autoimmune thyroid disease (ATD) is essentially due to the presence of simultaneously occurring autoimmune gastrointestinal diseases.
Anemia occurs in 82% of patients with Autoimmune Thyroid Disease (AITD) and Autoimmune Atrophic Gastritis (AIAG). In the patients with AITD studied, about one third had AIAG, which was diagnosed also in young patients. The presence of anemia, even microcytic, was suggestive of undiagnosed AIAG. The increased frequency of chronic anemia in patients with autoimmune thyroid disease (AITD) is essentially due to the presence of autoimmune gastrointestinal diseases occurring simultaneously.
The classical paradigm of autoimmune pathogenesis involving a specific genetic makeup and exposure to environmental triggers has been challenged by the addition of a third element: the loss of intestinal barrier function.
This new paradigm implies that, once the autoimmune process is activated, it is not self-perpetuating; rather it can be modulated or even reversed by preventing the continuous interplay between genes and environment.
Recognition of the bacterial interaction with the intestinal barrier dysfunction allows new therapeutic strategies aimed at re-establishing the intestinal barrier function to be offered as innovative, unexplored approaches for the treatment of these devastating diseases.
Autoimmune process can be arrested if the interplay between genes and environmental triggers is prevented by Re-Establishing Intestinal Barrier Function.
The primary functions of the gastrointestinal tract have traditionally been perceived to be limited to the digestion and absorption of nutrients and electrolytes, and water. A more attentive analysis of the anatomic and functional arrangement of the gastrointestinal tract suggests that another extremely important function of this organ is its ability to regulate the trafficking of macromolecules between the environment and the host through a barrier mechanism. Together the neuroendocrine network with the intestinal epithelial barrier, and its intercellular tight junctions, controls the equilibrium between tolerance and immunity to nonself-antigens. When the finely tuned trafficking of macromolecules is dysregulated, neurotransmitters can no longer control pro-inflammatory cytokines and both intestinal and extraintestinal autoimmune disorders can occur.
This new paradigm subverts traditional theories underlying the development of autoimmunity, which are based on molecular mimicry and/or the bystander effect, and suggests that the autoimmune process can be arrested if the interplay between genes and environmental triggers is prevented by re-establishing intestinal barrier function.
Understanding the role of bacteria and the intestinal barrier in the pathogenesis of autoimmune thyroid diseased and autoimmune gastrointestinal disease requires understanding multiple elements contributing to the onset of these conditions.
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