Canine chronic inflammatory enteropathy (CIE) is one of the most common chronic gastrointestinal diseases affecting dogs worldwide. Genetic and environmental factors, as well as intestinal microbiota and dysregulated host immune responses, participate in this multifactorial disease. Despite advances explaining the immunological and molecular mechanisms involved in CIE development, the exact pathogenesis is still unknown. This review compiles the latest reports and advances that describe the main molecular and cellular mechanisms of both the innate and adaptive immune responses involved in canine CIE pathogenesis. Future studies should focus research on the characterization of the immunopathogenesis of canine CIE in order to advance the establishment of biomarkers and molecular targets of diagnostic, prognostic, or therapeutic utility.

Cystic echinococcosis (CE) is a globally distributed zoonotic disease caused by Echinococcus granulosus sensu lato, forming fluid-filled cysts in humans and livestock. These cysts consist of three layers: an inner germinal layer and a middle laminar layer of parasitic origin, and an outer adventitial layer derived from the host’s immune response. The adventitial layer typically contains immune cells such as T and B lymphocytes, macrophages, and other inflammatory cells. Notably, differences have been reported in the cellular composition of this layer depending on the host species. However, the variation in calprotectin expression—a protein specific to phagocytes—between cattle and sheep CE cysts has not been previously described. This study assessed calprotectin expression using immunohistochemistry with anti-calprotectin antibodies on adventitial tissue sections from cattle and sheep CE cysts. The results showed a significantly higher calprotectin expression in the adventitial layer of cattle cysts compared to sheep. This difference was not associated with the fertility or anatomical location of the cysts. These findings suggest that the host species influences the level of calprotectin expression in the adventitial layer, contributing to our understanding of host-specific immune responses in CE.

Canine chronic enteropathy (CE) is a gastrointestinal disorder characterized by persistent or recurrent digestive symptoms lasting more than three weeks. It shares similarities with human inflammatory bowel disease but its immunopathogenesis remains poorly characterized in dogs. The aim of this study was to characterize the local and systemic immune profile of dogs with CE by assessing cytokine and chemokine expression in serum and intestinal tissue, as well as the mRNA expression of immune-related receptors such as integrins, chemokine receptors, and cytokines. Duodenal biopsies and blood samples were collected from five dogs diagnosed with a CE and five healthy controls. Serum concentrations of cytokines and chemokines were determined by multiplex ELISA, and mRNA expression in the intestinal mucosa was analyzed by quantitative PCR. Dogs with a CE showed increased expression of pro-inflammatory cytokines, including TNF-α and IFN-γ, and increased concentrations of chemokines such as CXCL10 and CCL2 in both serum and tissue samples. Increased mRNA expression of the chemokine receptor CCR9 and the adhesion molecule MAdCAM-1 were also observed in intestinal samples. These findings provide new insights into the immune response involved in CE and may aid the development of future diagnostic biomarkers and targeted therapies for canine chronic enteropathies.

Background: Continuous insulin infusion protocols are essential for managing decompensated diabetic dogs, but comparative data between variable and fixed infusion rates are limited. Methods: This prospective observational study evaluated the glycemic response of 21 diabetic dogs treated with a fixed-dose continuous-rate infusion (CRI) of regular insulin at 0.05 IU/kg/h for 12 h. Capillary blood glucose was measured hourly. Statistical analyses included Wilcoxon signed-rank tests, Friedman test, Mann–Whitney U, and Kruskal–Wallis tests. Results: A significant reduction in glucose concentration occurred during the first five hours of infusion (p < 0.0001), followed by a stabilization phase with no further significant changes. No differences in glycemic response were found by sex or breed. The protocol was well tolerated, with no hypoglycemic events observed. Conclusions: A fixed-dose CRI of 0.05 IU/kg/h offers a safe and effective option for acute glycemic control in diabetic dogs, including those with early ketoacidosis. The standardized approach simplifies management without compromising efficacy and supports its inclusion in emergency treatment protocols.

Protein-losing nephropathy (PLN) involves a heterogeneous group of pathologies leading to selective glomerular damage and development of renal disease. ICGN, the main cause of PLN, requires immunosuppressive treatment. However, the scientific evidence in veterinary medicine on immunosuppressive therapeutic schemes in this condition is limited. The aim of this study is to describe the clinical and paraclinical evolution of five dogs with PLN, presumably associated with ICGN, treated with chlorambucil as immunosuppressive monotherapy. Suspected IGCN was established by the presence of a urine protein–creatinine ratio (UPC) ≥ 3 without response to standard therapy, hypoalbuminemia < 2, or progressive azotemia. Patients were treated with a dosage range of chlorambucil from 0.16 to 0.4 mg/kg (mean 0.25 mg/kg) every 24 h as the sole immunosuppressant. In the end, 4/5 patients showed significant clinical improvement, 3/3 had resolution of the nephrotic syndrome, 5/5 had a sustained decrease in UPC values during follow-up and no relevant adverse effects were observed. In this report, chlorambucil proved to be a well-tolerated and potentially effective monotherapy for immune-mediated PLN in dogs.