We identified a key signaling pathway associated with the adrenocortical autograft regeneration that has not been elucidated previously. Using the RNAscope technology, a novel in situ RNA hybridization assay, we found transient upregulation of Desert hedgehog (Dhh), a key signaling factor, and downregulation of Sonic hedgehog (Shh) in the process of graft regeneration. Interestingly, it had been reported that Dhh expression is localized to the gonadal tissues and its expression in the adrenal cortex has not been reported yet. Conversely, Shh-positive cells are known candidates for stem and progenitor cells in the adrenal cortex, but they exhibit little or no involvement in the process of adrenocortical graft regeneration. In addition to the previously known function of DHH in gonads, our findings suggest that it may further participate in the process of adrenocortical autograft regeneration. Our findings provide useful insights in the implementation of adrenal graft implantation and stem cell-derived adrenocortical cell generation. In this article, we will review our findings, the development of adrenal cortex, stem and progenitor cells, and other aspects.
The gut microbiota resides in the human gastrointestinal tract, maintaining a certain homeostatic balance. Recent advancements in next-generation sequencing have accelerated our understanding of the human gut microbiota, which is established after birth (or in utero) and starts to resemble the microbiota of an adult by the age of three years. Various factors affect its composition, and imbalances thereof have been associated with an increased risk of disease during both childhood and adulthood. Therefore, a deeper understanding of the establishment of the gut microbiota during childhood is critical for human health promotion. However, due to the numerous, complex factors affecting the gut microbiome, the exact etiology remains unknown. Herein, we discuss the impact of mode of delivery and feeding type on neonate gut microbiota.
Follicular pancreatitis is characterized by the presence of many intrapancreatic lymphoid follicles with reactive germinal centers. However, its clinicopathological features and cause have not yet been established. We assessed the clinicopathological features with follicular pancreatitis who underwent surgery. This study included 3 patients with a pancreatic mass. Histopathological study of the resected pancreatic mass revealed that abundant lymphoid follicles with reactive germinal centers were present in both periductal regions and were diffused in parenchyma. Podoplanin (Th17 marker)-expressing lymphocytes were present in lymphoid follicles of those with follicular pancreatitis, whereas these were absent in normal lymph nodes and in lymphoid follicles of those with IgG4-related autoimmune pancreatitis (AIP). RNA digital counting assay clearly demonstrated that the expression counts of 20 genes, including dendritic cells and lymphoid follicles markers, and related cytokines were significantly higher in follicular pancreatitis than in IgG4-related AIP (p<0.01). The expression of IL23A, which are genes related to Th17, was high. This study shows that follicular pancreatitis is a histopathologically and immunologically distinct disease entity of pancreatitis and is characterized by upregulated Th17 expression.