Epidemiology: Open Access
Open Access

IBD refers to a set of inflammatory disorders of the colon and small intestine, the most common of which being Crohn's disease and ulcerative colitis. Crohn's disease affects the small and large intestines, as well as the mouth, oesophagus, stomach, and anus, whereas ulcerative colitis affects mostly the colon and rectum [1, 2, 3].

In dogs, IBD is assumed to be caused by a combination of host genetics, the intestinal milieu, environmental factors, and the immune system. However, there is a growing consensus that the term "chronic enteropathy" rather than "inflammatory bowel disease" should be used in dogs because the dogs' response to treatment differs from that of people. In contrast to humans with IBD, who frequently require immunosuppressive treatment, many dogs respond to merely dietary changes. When dietary adjustments are insufficient, some dogs may require immunosuppressive or antibiotic medication. After other diseases that might cause vomiting, diarrhoea, and abdominal pain in dogs have been ruled out, intestinal biopsies are frequently performed to determine what type of inflammation is present (lymphoplasmacytic, eosinophilic, or granulomatous). Low blood levels of cobalamin have been found to be a risk factor for bad outcomes in dogs [4, 5, 6].

Signs and symptoms

Despite the fact that Crohn's and UC are two completely distinct diseases, both can cause abdominal pain, diarrhoea, rectal bleeding, severe internal cramps/muscle spasms in the pelvic region, and weight loss. The most common extraintestinal consequence of inflammatory bowel disease is anaemia [7, 8]. Arthritis, pyoderma gangrenosum, primary sclerosing cholangitis, and non-thyroidal sickness syndrome are all associated symptoms or disorders (NTIS) [9]. There have also been links to deep vein thrombosis (DVT) [10] and bronchiolitis obliterans organising pneumonia (BOOP) [11]. The most common method of diagnosis is to examine inflammatory markers in the stool, followed by a colonoscopy and biopsy of pathological lesions.

Causes

IBD is a complicated disease that results from the combination of environmental and genetic variables in the intestine, causing immune reactions and inflammation [1].

Diet

Increased intake of fruits and vegetables, reduced intake of processed meats and refined carbohydrates, and a preference for water for hydration were all linked to a lower risk of active IBD symptoms in a 2022 study, though increased intake of fruits and vegetables alone did not reduce the risk of Crohn's disease symptoms.

Dietary trends have been linked to an increased risk of ulcerative colitis. Subjects in the highest tertile of the healthy eating pattern, in instance, had a 79% decreased incidence of ulcerative colitis.

Gluten sensitivity is widespread in people with IBD, and it's linked to flare-ups. Gluten sensitivity was found in 23.6 percent of Crohn's disease patients and 27.3 percent of ulcerative colitis patients, respectively.

A high-protein diet, particularly animal protein, and/or a highsugar diet may increase the incidence of relapses and inflammatory bowel disease.

Microbiota

Alterations in the gut microbiome may lead to inflammatory gut disorders as a result of microbial symbiosis and immunity [12]. The biodiversity of commensal bacteria in IBD patients has been reported to be 30–50 percent lower, with declines in Firmicutes (specifically Lachnospiraceae) and Bacteroidetes. IBD-affected people are more likely than unaffected people to have been administered antibiotics in the 2–5 years leading up to their diagnosis, providing more evidence of the importance of gut flora in the pathogenesis of inflammatory bowel disease [13]. Environmental variables such as concentrated milk fats (a common ingredient in processed foods and confectionery) or oral drugs such as antibiotics and oral iron preparations can change enteral flora [14]. The mucosal microbiota in the large intestine of IBD patients with active inflammation was linked to host epigenome alterations that were pro-inflammatory [15] Large worldwide investigations, on the other hand, have failed to establish a single microbiological biomarker of IBD, indicating that it is not caused by a single microbe [16].

Intestinal barrier breach

The loss of intestinal epithelial integrity is a critical pathogenic factor in IBD. The innate immune system's dysfunction, which is caused by aberrant signalling through immune receptors known as toll-like receptors (TLRs), which initiates an immune response to molecules shared by various pathogens, promotes to acute and chronic inflammatory processes in IBD colitis and cancer. Changes in the gut microbiota composition are a significant environmental element in the development of IBD. Damage to the intestinal epithelium is caused by changes in the intestinal microbiota, which trigger an inappropriate (uncontrolled) immune response. Breach of this crucial barrier (the intestinal epithelium) allows for more microbial invasion, which triggers more immunological responses. IBD is a complex disease that is exacerbated by an overactive immune response to gut microbiota, resulting in epithelial barrier dysfunction [17].

Genetics

For almost a century, scientists have known that IBD includes a genetic component [18]. Research of ethnic groupings (e.g., Ashkenazi Jews, Irish), familial clustering, epidemiological studies, and twin studies have all added to our understanding of genetics. Understanding of the genetic underpinnings has greatly expanded with the advent of molecular genetics, particularly in the last decade [19]. NOD2 was the first gene to be identified to IBD in 2001. Since then, genome-wide association studies have added to our understanding of the disease's genetics and pathology. There are now over 200 single nucleotide polymorphisms (SNPs or "snips") that have been linked to IBD risk [20]. In 2012, one of the most comprehensive genetic studies of IBD was released. In Crohn's disease and ulcerative colitis, the study explained more variance than previously reported [19] The findings revealed that in inflammatory bowel illnesses, commensal microbiota are transformed in such a way that they act as pathogens. Other research suggests that mutations in IBD-associated genes may disrupt cellular activity and interactions with the microbiome, which are necessary for proper immune responses. MicroRNA dysregulation has been linked to IBD and the promotion of colorectal cancer in numerous studies. A small group used IBD patient biopsy material to begin single-cell RNA sequencing analysis in the quest for therapeutic targets around 2020.

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