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Published on: September 22, 2019
Chronic skin damage induces small intestinal damage via IL-13-induced apoptosis
Rina Tanemoto1, Masaaki Higashiyama1, Akira Tomioka1
1Department of Gastroenterology, National Defense Medical College, Saitama, Japan.
Abstract:
The gut-skin axis has recently been widely recognized, and both the gut and skin have been found to affect each other through a bidirectional connection; however, the precise mechanisms remain to be elucidated. Therefore, we aimed to investigate the effects of chronic skin damage (CSD) on mouse intestines. Following the CSD model, 4% sodium dodecyl sulfate was applied to the back-shaved murine skin six times for 2 weeks after tape stripping. The small and large intestines were analyzed histologically and immunologically, respectively. Intestinal permeability was measured using fluorescein isothiocyanate-conjugated-dextran. The role of interleukin-13 (IL-13) in the ileum was investigated using an anti-IL-13 antibody. Apoptotic intestinal cells were analyzed using TUNEL staining. Villus atrophy was observed in the small intestine in the CSD model, along with increased permeability. Mast cells, but not T cells, eosinophils, or innate lymph cell-2, were increased in the intestinal mucosa. However, no significant changes were observed in the large intestine. mRNA expression of IL-13 was increased only in the ileum of the CSD model. Apoptotic intestinal epithelial cells were significantly increased in the ileum of the CSD model. Administration of an anti-IL-13 antibody ameliorated the intestinal damage caused by CSD, along with decreased apoptotic cells and mast cell infiltration. Skin damage causes morphological changes in the small intestine, accompanied by increased intestinal permeability, possibly through the IL-13-induced apoptosis of mast cells in the epithelium. Surfactant-mediated mechanical skin damage can cause a leaky gut.
Insights
Chronic skin damage in mice led to small intestine changes, including villus atrophy and increased permeability. Interleukin-13 (IL-13) mediated this damage by increasing mast cell apoptosis, suggesting skin issues can cause a "leaky gut".
Area of Science:
- Gastroenterology
- Dermatology
- Immunology
Background:
- The gut-skin axis describes bidirectional communication between the gut and skin.
- Mechanisms linking skin damage to gut health require further investigation.
Purpose of the Study:
- To investigate the impact of chronic skin damage (CSD) on mouse intestines.
- To elucidate the role of interleukin-13 (IL-13) in CSD-induced intestinal alterations.
Main Methods:
- A chronic skin damage model was established using sodium dodecyl sulfate and tape stripping.
- Histological and immunological analyses were performed on mouse intestines.
- Intestinal permeability, IL-13 levels, and apoptosis were assessed.
Main Results:
- CSD induced villus atrophy and increased intestinal permeability in the small intestine.
- Mast cell infiltration and IL-13 mRNA expression increased in the ileum.
- IL-13 blockade ameliorated intestinal damage, reduced apoptosis, and decreased mast cell infiltration.
Conclusions:
- Chronic skin damage can lead to significant small intestine morphological changes and increased permeability.
- Interleukin-13 plays a key role in mediating CSD-induced intestinal damage, potentially via mast cell apoptosis.
- These findings highlight that skin damage can compromise gut barrier function, resulting in a "leaky gut".
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