Gut: Key Element on Immune System Regulation

Abstract The gut is the main organ that mediates the contact between antigens with our organism, controlling the immune response against environmental factors, such as microbiota and food. Innate lymphoid cells participate in the gut-associated lymphoid tissue (GALT) maturation during the prenatal and early postnatal periods. After birth, breast milk provides the essential elements for the continuity of development of this tissue, leading to structural changes and healthy microbiota installation. The microbiota participates in the organogenesis of the GALT, as in the formation of intestinal villi, stimulating the proliferation of stem cells and maintaining the integrity of epithelial barrier. Foods are also involved in maturation of the GALT, where the protein source depletion reduced the number of resident lymphocytes. This unique microenvironment present in the intestinal lamina propria (LP) and mesenteric lymph nodes (mLN) induce tolerance to innocuous antigens from the diet, known as Oral Tolerance. Antigens sampled by intestinal epithelium cells are transferred to specialized dendritic cells, residing in the LP, which migrate to the mesenteric lymph nodes where they participate in the induction of regulatory T cells (Treg). Understanding these phenomena may establish the intestinal mucosa as a tool in therapy of inflammatory bowel diseases and immunological disorders.

The role of potassium channels in the endothelial dysfunction induced by periodontitis

Abstract Objective: Periodontitis is associated with endothelial dysfunction, which is clinically characterized by a reduction in endothelium-dependent relaxation. However, we have previously shown that impairment in endothelium-dependent relaxation is transient. Therefore, we evaluated which mediators are involved in endothelium-dependent relaxation recovery. Material and methods: Rats were subjected to ligature-induced experimental periodontitis. Twenty-one days after the procedure, the animals were prepared for blood pressure recording, and the responses to acetylcholine or sodium nitroprusside were obtained before and 30 minutes after injection of a nitric oxide synthase inhibitor (L-NAME), cyclooxygenase inhibitor (Indomethacin, SC-550 and NS- 398), or calcium-dependent potassium channel blockers (apamin plus TRAM- 34). The maxilla and mandible were removed for bone loss analysis. Blood and gingivae were obtained for C-reactive protein (CRP) and myeloperoxidase (MPO) measurement, respectively. Results: Experimental periodontitis induces bone loss and an increase in the gingival MPO and plasmatic CRP. Periodontitis also reduced endothelium-dependent vasodilation, a hallmark of endothelial dysfunction, 14 days after the procedure. However, the response was restored at day 21. We found that endothelium-dependent vasodilation at day 21 in ligature animals was mediated, at least in part, by the activation of endothelial calcium-activated potassium channels. Conclusions: Periodontitis induces impairment in endothelial-dependent relaxation; this impairment recovers, even in the presence of periodontitis. The recovery is mediated by the activation of endothelial calcium-activated potassium channels in ligature animals. Although important for maintenance of vascular homeostasis, this effect could mask the lack of NO, which has other beneficial properties.