Isthmic progenitors, tissue-specific stem cells in the stomach corpus, maintain mucosal homeostasis by balancing between proliferation and differentiation to gastric epithelial lineages. The progenitor cells rapidly adopt an active state in response to mucosal injury. However, it remains unclear how the isthmic progenitor cell niche is controlled during the regeneration of damaged epithelium. We recapitulated tissue recovery process after acute mucosal injury in the mouse stomach. BrdU incorporation was utilized to trace newly generated cells during the injury and recovery phases. To define epithelial lineage commitment process during recovery, we performed single cell RNA-sequencing (scRNA-seq) on epithelial cells from the mouse stomachs. We validated the effects of amphiregulin (AREG) on mucosal recovery, utilizing recombinant AREG treatment or AREG deficient mice. We determined that an EGFR ligand, AREG, can control progenitor cell lineage commitment. Based on the identification of lineage-committed subpopulations in the corpus epithelium through scRNA-seq and BrdU incorporation, we showed that isthmic progenitors mainly transition into short-lived surface cell lineages, but are less frequently committed to long-lived parietal cell lineages in homeostasis. However, mucosal regeneration after damage directs the lineage commitment of isthmic progenitors towards parietal cell lineages. During recovery, AREG treatment promoted repopulation with parietal cells, while suppressing surface cell commitment of progenitors. In contrast, TGF-alpha did not alter parietal cell regeneration, but did induce expansion of surface cell populations. AREG deficiency impairs parietal cell regeneration, but increases surface cell commitment. These data demonstrate that different EGF receptor ligands can distinctly regulate isthmic progenitor-driven mucosal regeneration and lineage commitment.

Research on the microenvironment associated with gastric carcinogenesis has focused on cancers of the stomach and often underestimates premalignant stages such as metaplasia and dysplasia. Since epithelial interactions with T cells, macrophages, and type 2 innate lymphoid cells (ILC2s) are indispensable for the formation of precancerous lesions in the stomach, understanding the cellular interactions that promote gastric precancer warrants further investigation. Although various types of immune cells have been shown to play important roles in gastric carcinogenesis, it remains unclear how stromal cells such as fibroblasts influence epithelial transformation in the stomach, especially during precancerous stages. Fibroblasts exist as distinct populations across tissues and perform different functions depending on the expression patterns of cell surface markers and secreted factors. In this review, we provide an overview of known microenvironmental components in the stroma with an emphasis on fibroblast subpopulations and their roles during carcinogenesis in tissues including breast, pancreas, and stomach. Additionally, we offer insights into potential targets of tumor-promoting fibroblasts and identify open areas of research related to fibroblast plasticity and the modulation of gastric carcinogenesis.

Entamoeba (E.) histolytica is a major global health concern as the causative agent of amoebic colitis, yet research is hindered by the lack of an ideal animal model. While E. muris has been traditionally considered non-pathogenic, our study demonstrates that it induces a colitis-like pathology in BALB/c mice, making it a promising model for studying E. histolytica infection. Using a fecal-oral infection route, we confirmed successful E. muris colonization, leading to colonic inflammation characterized by early CD4 + T-cell infiltration and FOXP3 + regulatory T-cell recruitment. We further demonstrate that T-cell immunity is essential for E. muris colonization, as T-cell-depleted BALB/c mice and T-cell-deficient BALB/c nude mice failed to support persistent infection. Additionally, infection disrupts epithelial homeostasis, impairing goblet cell generation, and induces significant shifts in gut microbiota composition, notably reducing beneficial Firmicutes species. Collectively, these findings demonstrate that E. muris infection induces inflammation and microbiota alterations, mirroring critical aspects of amoebic colitis, reinforcing its value as a model for studying E. histolytica pathogenesis and host–parasite interactions.

Ferret coronavirus infection in a domestic ferret (Mustela putorius furo) coronavirus infection;ferret;immunohistochemistry;peritonitis; A female domestic ferret (Mustela putorius furo) presented to a veterinary clinic with a clinical history of anorexia and poor body condition. Due to gradual deterioration of the body condition, explorative laparotomy was performed. Diffusely, the mesentery was severely thickened and adhered with prominent mesenteric lymph nodes. A portion of the mesentery and mesenteric lymph nodes were biopsied and fixed. Microscopic analysis revealed severe pyogranulomatous peritonitis and lymphadenitis, but staining revealed no bacterial organisms. However, immunohistochemistry for feline coronavirus exhibited strong immunoreactivity, primarily in the macrophages. Based on these results, the case was diagnosed as ferret coronavirus infection.

An 8-y-old, castrated male Korean Shorthair cat was presented to a veterinary clinic for evaluation of a cutaneous mass on the left inner thigh. Microscopic examination revealed a poorly circumscribed dermal neoplasm composed of poorly granulated, pleomorphic neoplastic mast cells with frequent cell-in-cell structures. Notably, viable neoplastic mast cells were engulfed by large macrophages, indicating a specific form of the cell-in-cell phenomenon. Immunohistochemistry for c-KIT, IBA1, and cleaved caspase-3 was used to support the diagnosis. To our knowledge, cell-in-cell phenomenon has not been previously described in feline cutaneous mast cell tumors, nor has the clinical outcome of such cases been reported