A research team at the University of Miyazaki has succeeded in clarifying the mechanism by which antibiotic administration during childhood increases the risk of developing allergies.
A living body is equipped with an immune mechanism that eliminates foreign substances that have invaded the body, but at the same time, it also has a mechanism called immune tolerance that blocks adverse immune responses.For example, in the gastrointestinal tract, gastrointestinal mucosal immune tolerance is established to block immune reactions to ingested food.However, when digestive tract mucosal immune tolerance is broken, it is believed to lead to the onset of food allergy.
On the other hand, taking antibiotics has been shown to cause gastrointestinal flora abnormalities, and infants who used antibiotics by the age of 2 years had a significantly higher risk of developing allergic diseases at the age of 5 years. has been reported.Based on the above, the present study investigated the possibility that abnormal gastrointestinal microflora induced by taking antibiotics in childhood disrupts gastrointestinal mucosal immune tolerance and increases the risk of developing allergies.
First, mice deficient in dendritic cells, a type of leukocyte present in mucosal tissue, do not establish gastrointestinal mucosal immune tolerance, and mucosal tissue dendritic cells are essential for the establishment of gastrointestinal mucosal immune tolerance. I found
Next, when we investigated the effects of taking antibiotics during childhood, we found abnormal gastrointestinal flora indicating a decrease in the indigenous bacteria of the gastrointestinal tract. Cells were found to produce less tumor necrosis factor-like ligand 1A (TL1A). TL1A enhances the immunosuppressive function of mesenteric lymph node mucosal dendritic cells by enhancing the production of colony-stimulating factor 3 by type 2 innate lymphocytes.In other words, it is clear that taking antibiotics at a young age leads to loss of immunosuppressive function of mesenteric lymph node mucosal tissue dendritic cells through decreased TL1A production, resulting in the breakdown of gastrointestinal mucosal immune tolerance. became.
This achievement, which clarified the mechanism of the breakdown of gastrointestinal mucosal immune tolerance, is expected to lead to the development of new treatments for allergies.
Paper information:[Cell Reports] Gut dysbiosis promotes the breakdown of oral tolerance mediated through dysfunction of mucosal dendritic cells
