The mucosal immune system may play a critical role in the pathogenesis of small intestinal enteropathies. The aim of the current study was to assess mucosal immune cell populations in dogs with inflammatory bowel disease (IBD), idiopathic antibiotic-responsive diarrhea (ARD), and adverse reactions to food (FR). Endoscopic biopsies were performed of the duodenum of dogs with these conditions and from a group of dogs without enteric disease. Additional control samples were collected after death from other dogs that did not have evidence of enteric disease. Immunohistochemistry and computer-aided morphometry were used to assess the distribution of immune cell subsets in both lamina propria and intestinal epithelium. Compared with controls, dogs with ARD had increased numbers of lamina propria immunoglobulin (Ig) A plasma cells and CD4 cells. More marked alterations were noted in dogs with IBD, with significant increases in lamina propria IgG plasma cells, T cells (CD3), CD4 cells, mac-rophages, and neutrophils, but with reduced mast cell numbers. Increased intraepithelial CD3 T cells were also present in the dogs with IBD, compared with controls. However, lamina propria and epithelial populations were unaltered in dogs with FR when compared with controls. The altered mucosal immune cell populations observed in dogs with ARD or IBD may reflect an underlying immunologic pathogenesis in these disorders.
Immunologic variables in dogs with eosinophilic bronchopneumopathy (EBP) have not been extensively evaluated. The aim of this study was to determine immunoglobulin (Ig) concentrations and to perform phenotypic subtyping of lymphocytes in the bronchoalveolar lavage fluid (BALF) and peripheral blood (PB) of 12 dogs with EBP at the time of diagnosis (TD) and to compare these data with those obtained in healthy dogs, as well as in EBP dogs after antibiotic therapy (TAB) and during corticosteroid treatment (TM). Matched samples of serum and BALF were used to determine Ig concentrations (IgG, IgM, and IgA) by capture enzyme-linked immunosorbent assay (ELISA), from which a secretory index (SI) was calculated. Lymphocyte subpopulations were studied in the BALF and PB by flow cytometry. Log values of BALF IgM and IgA were significantly higher (0.64 Ϯ 0.05 and 1.06 Ϯ 0.13, respectively) in EBP dogs at TD than in controls and then tended to decrease at TM (0.55 Ϯ 0.03 and 1.02 Ϯ 0.17, respectively). A calculated SI for IgA was not significantly increased. In the BALF of dogs with EBP, the CD4 : CD8 was significantly (P Ͻ .05) higher (22.6 Ϯ 30.3) than in controls (3.2 Ϯ 1.9), due to significantly higher CD4 ϩ T cells and lower CD8 ϩ T cells. At TM, the BALF T-cell percentages returned to normal (2.4 Ϯ 0.6). We propose that the influx of eosinophils into the airway of dogs with EBP is at least in part mediated by cytokines derived from CD4 ϩ T cells. Further studies of canine cytokines and chemokines will help determine whether canine EBP involves type I hypersensitivity mechanisms regulated by Th2 lymphocytes.
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