The aim of our study was to investigate histopathologically the incidence of gastrointestinal tract tumours in dogs in the Czech Republic in relation to their age, sex and breed. In total, 29 gastric and 45 intestinal tumours from 3827 gastrointestinal tract biopsies were investigated. The average age of dogs with gastric lymphoma, adenocarcinoma, and other mesenchymal tumours was 7.3 years, 9.5 years, and > 10 years, respectively. Breed predisposition to adenocarcinoma was evidenced in the Belgian Shepherd and Leonberger, to lymphoma in the Doberman (P < 0.01). The most frequent site of adenocarcinoma was antrum pyloricum (66.7%); lymphomas involved gastric wall diffusely. The average age of dogs with intestinal adenoma, adenocarcinoma, lymphoma, leiomyoma or leiomyosarcoma and carcinoid was 7.5, 8.5, 8.5, 12, and 14 years, respectively. The age predisposition to intestinal adenoma and lymphoma was 7-8 years (P < 0.01) and to adenocarcinoma 7-8 years (P < 0.05); mesenchymal tumours occurred at the age of 11-12 years (P < 0.01). Breed predisposition to intestinal adenoma was evidenced in the Pug, Leonberger and English Setter (P < 0.01), to adenocarcinoma in the English Setter (P < 0.01) and Hovawart (P < 0.05), to lymphoma in the Doberman and Hovawart (P < 0.05). The most frequent site of occurrence of intestinal tumours was the colorectal region. The study revealing breed, sex and age predisposition to gastrointestinal tumours in dogs has not been described yet in the literature.
Protists are a normal component of mammalian intestinal ecosystems that live alongside, and interact with, bacterial microbiota. Blastocystis, one of the most common intestinal eukaryotes, is reported as a pathogen that causes inflammation and disease, though health consequences likely vary depending on host health, the gut ecosystem, and genetic diversity. Accumulating evidence suggests that Blastocystis is by and large commensal. Blastocystis is more common in healthy individuals than those with immune mediated diseases such as Inflammatory Bowel Diseases (IBD). Blastocystis presence is also associated with altered composition and higher richness of the bacterial gut microbiota. It is not clear whether Blastocystis directly promotes a healthy gut and microbiome or is more likely to colonize and persist in a healthy gut environment. We test this hypothesis by measuring the effect of Blastocystis ST3 colonization on the health and microbiota in a rat experimental model of intestinal inflammation using the haptenizing agent dinitrobenzene sulfonic acid (DNBS). We experimentally colonized rats with Blastocystis ST3 obtained from a healthy, asymptomatic human donor and then induced colitis after 3 weeks (short term exposure experiment) or after 13 weeks (long term exposure experiment) and compared these colonized rats to a colitis-only control group. Across experiments Blastocystis ST3 colonization alters microbiome composition, but not richness, and induces only mild gut inflammation but no clinical symptoms. Our results showed no effect of short-term exposure to Blastocystis ST3 on gut inflammation following colitis induction. In contrast, long-term Blastocystis exposure appears to promote a faster recovery from colitis. There was a significant reduction in inflammatory markers, pathology 2 days after colitis induction in the colonized group, and clinical scores also improved in this group. Blastocystis colonization resulted in a significant reduction in tumor necrosis factor alpha (TNFα) and IL-1β relative gene expression, while expression of IFNγ and IL17re/17C were elevated. We obtained similar results in a previous pilot study. We further found that bacterial richness rebounded in rats colonized by Blastocystis ST3. These results suggest that Blastocystis sp. may alter the gut ecosystem in a protective manner and promote faster recovery from disturbance.
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