RESUMEN
Recent evidence of gut microbiota dysbiosis in the context of psoriasis and the increased cooccurrence of inflammatory bowel disease and psoriasis suggest a close relationship between skin and gut immune responses. Using a mouse model of psoriasis induced by the Toll-like receptor (TLR) 7 ligand imiquimod, we found that psoriatic dermatitis was accompanied by inflammatory changes in the small intestine associated with eosinophil degranulation, which impaired intestinal barrier integrity. Inflammatory responses in the skin and small intestine were increased in mice prone to eosinophil degranulation. Caco-2 human intestinal epithelial cells were treated with media containing eosinophil granule proteins and exhibited signs of inflammation and damage. Imiquimod-induced skin and intestinal changes were attenuated in eosinophil-deficient mice, and this attenuation was counteracted by the transfer of eosinophils. Imiquimod levels and the distribution of eosinophils were positively correlated in the intestine. TLR7-deficient mice did not exhibit intestinal eosinophil degranulation but did exhibit attenuated inflammation in the skin and small intestine following imiquimod administration. These results suggest that TLR7-dependent bidirectional skin-to-gut communication occurs in psoriatic inflammation and that inflammatory changes in the intestine can accelerate psoriasis.
Asunto(s)
Degranulación de la Célula , Modelos Animales de Enfermedad , Eosinófilos , Imiquimod , Intestino Delgado , Psoriasis , Receptor Toll-Like 7 , Animales , Receptor Toll-Like 7/metabolismo , Receptor Toll-Like 7/genética , Psoriasis/patología , Psoriasis/metabolismo , Ratones , Eosinófilos/metabolismo , Eosinófilos/inmunología , Humanos , Intestino Delgado/patología , Intestino Delgado/metabolismo , Piel/patología , Piel/metabolismo , Inflamación/patología , Inflamación/metabolismo , Ratones Noqueados , Células CACO-2 , Glicoproteínas de MembranaRESUMEN
An 11-year-old intact female Pomeranian dog was referred for jaundice, anorexia, and vomiting. The blood analysis revealed increased alanine aminotransferase, alkaline phosphatase, and gamma-glutamyl transpeptidase. The serum canine pancreatic lipase immunoreactivity was within the normal reference range. The radiography revealed no significant findings. On ultrasound, the gallbladder was enlarged with a markedly distended common bile duct (CBD) measuring up to 6 mm in diameter. The pancreas had an irregular contour, a hypoechoic peripheral rim, multiple hyperechoic foci with acoustic shadowing, and showed increased echogenicity of the adjacent mesentery. Based on these results, an extrahepatic biliary obstruction secondary to the presumed chronic pancreatitis was diagnosed. The computed tomography (CT) images showed a hypoattenuating pancreatic parenchyma compared to the liver in the early phase, as well as multiple calcifications. A laparotomy was performed to reserve the patency of the CBD. The histopathological examination of the pancreas revealed exocrine pancreatic adenocarcinoma. While various appearances of exocrine pancreatic adenocarcinoma on CT have been reported in humans, CT features of pancreatic adenocarcinoma have not been well-established in dogs. The purpose of this report is to describe the atypical imaging features of pancreatic adenocarcinoma that are similar to those of chronic pancreatitis in a dog.
