Özet:

The intestinal tract has developed various strategies that allow a symbiotic relationship with the microbiota and restrict the invasion of microorganisms. Toll-like receptors (TLRs) are expressed in a variety of cell types, including macrophages, dendritic cells (DCs), T lymphocytes, and intestinal epithelial cells. TLRs act as pathogen recognition receptors (PRRs) that recognize pathogen-associated molecular patterns (MAMP) specific to pathogens and essential for their survival. Interactions between intestinal microbiota in humans and TLRs on intestinal epithelial cells and immune cells support the maintenance of the homeostasis of the immune system. TLR-related pathways regulate intrinsic metabolism in immune cells to allocate energy to immune response. Commensal bacteria are recognized as "non-pathogenic" after anti-inflammatory response with TLR2 activation. TLR4 expression is increased in adipose tissue, peripheral blood or muscle tissue samples of obese or type 2 diabetes patients and in adipose tissues of obese mice and is associated with insulin resistance. TLR5-deficient mice have been reported to be prone to developing the metabolic syndrome including insulin resistance and increased adiposity, which is associated with changes in microbiota composition. In addition, the beneficial effects of immunosuppression with the use of TLR antagonists continue to be investigated for metabolic and cardiovascular diseases. The intestinal microbiota changes due to genetics and environmental influences can cause host immune response problems and certain microbiota manipulations and reprogramming of microbiota in patients can offer accessible and promising treatment options. Therefore, it is important to understand how the relationship between the microbiota and the immune system will regulate metabolic parameters which could lead to advances in the treatment of metabolic diseases.

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