Background
The incidence of inflammatory bowel disease (IBD) is increasing worldwide, emphasizing the need of relevant models, as dogs spontaneously affected by IBD may be, for better knowledge of the disease’s physiopathology.
Methods
We studied 22 client-owned dogs suffering from IBD without protein loss and 14 control dogs. Biopsies were obtained from the duodenum, ileum, and colon. Inflammatory grade was assessed by histopathology, immunohistochemistry, and chemokine analysis. The expression of Toll-like receptors (TLR) in mucosa was immunohistochemically evaluated. Antibody levels against bacterial ligands (lipopolysaccharide [LPS] and flagellin) were measured in sera using enzyme-linked immunoassay.
Results
Dogs with IBD showed low to severe clinical disease. Histopathologically, the gut of dogs with IBD did not exhibit significant alterations compared with controls except in the colon. The number of CD3+ T lymphocytes was decreased in the ileum and colon of dogs with IBD compared with controls, whereas the numbers of Foxp3+, CD20+, and CD204+ cells were similar in the 2 groups. Three chemokines, but no cytokines, were detected at the protein level in the mucosa, and the disease poorly affected their tissue concentrations. Dogs with IBD exhibited higher serum reactivity against LPS and flagellin than controls but similar immunoreactivity against the receptors TLR4 and TLR5. In addition, TLR2 and TLR9 showed similar expression patterns in both groups of dogs.
Conclusions
Our data described dysregulated immune responses in dogs affected by IBD without protein loss. Despite fairly homogeneous dog cohorts, we were still faced with interindividual variability, and new studies with larger cohorts are needed to validate the dog as a model.
Interdigitating dendritic cell (IDC) hyperplasia
is considered a benign spontaneous condition occasionally observed in the lymph nodes of
mice. It has been rarely reported and, to the best of our knowledge, it has never been
characterized using immunohistochemistry. The present work describes a spontaneous IDC
hyperplasia case in a lymph node of a 16-week-old control female C57BL/6 mouse.
Microscopically, the lymph node architecture was completely effaced by the proliferation
of eosinophilic spindle cells with an abundant pale cytoplasm forming trabecule admixed
lymphocyte infiltrates. The spindle cell population was positive for F4/80, partially
positive for S100 calcium-binding protein A4 (S100A4), slightly positive for E-cadherin,
and negative for α-Smooth muscle actin (SMA) and cytokeratin. Lymphocytes were positive
for CD3, CD4, CD20 and negative for CD8. Spindle cells were considered to be originated
from the myeloid lineage, based on the immunohistochemistry (IHC) results, but their
precise origin remains unclear (IDC or macrophages); even if macrophage origin is most
likely based on F4/80 positivity, this remains to be further clarified using other
markers.
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