Multiple cystic intestinal duplications in a cat.

A 7-year-old, female European shorthair cat with a history of recurrent vomiting had a 2-cm cystic mass in the midjejunum. Cross-sectioning and histology revealed 3 separate cystic structures in the muscular layer, in addition to a regularly structured intestinal lumen. One cyst had a 3-layered wall consisting of a dysplastic mucosa, a regularly structured submucosa, and partly double-layered muscularis that sporadically contained neurons resembling a myenteric plexus. The remaining 2 cysts had similar structures except for granulation tissue lining the lumen. The lesion was diagnosed as multiple cystic duplications in the midjejunum, which is unknown to the veterinary literature to date.

Pathogenicity of Mycoplasma lipofaciens strain ML64 for turkey embryos.

Mycoplasma lipofaciens strain ML64, isolated from an egg of a northern goshawk (Accipiter gentilis), has been found to be pathogenic for chicken embryos causing mortality during the first 2 weeks of incubation. The same strain was inoculated in turkey embryos to evaluate its pathogenicity and its ability to be transmitted laterally in the hatchery. The strain was found to be pathogenic for turkey embryos, causing a high mortality (88.9%) during late incubation as well as haemorrhages of the legs, dwarfing, curled toes and a severe, multifocal, purulent to necrotizing bronchopneumonia. In addition, lateral transmission between turkey poults hatched from infected eggs and poults from non-infected controls was observed in the incubator.

Preventive effects of the probiotic Escherichia coli strain Nissle 1917 on acute secretory diarrhea in a pig model of intestinal infection.

Pretreatment with the probiotic Escherichia colistrain Nissle 1917 (EcN) was assessed in a pig model of intestinal infection to prevent acute secretory diarrhea. In the model 10(10) colony forming units of the porcine enterotoxigenic Escherichia coli Abbotstown (EcA) was given via orogastric tube to weaned piglets at day 21 postpartum (-EcN/+EcA group, n = 7). Forty-eight hours after challenge electrophysiological parameters of isolated intact jejunal epithelia were characterized in Ussing chambers. In agreement with clinical signs of diarrhea, tissues of challenged animals showed an overshoot of secretory response after stimulation of the cAMP-mediated second messenger pathway by forskolin, indicating higher excitability of chloride secretory systems under infected conditions. The data were compared with respective measurements from animals that got a daily dose of 10(10) cfu of the probiotic EcN over 10 days before EcA challenge (+EcN/+EcA group; n = 4), from a group that received only EcN (+EcN/-EcA; n = 4), or from a group that remained totally untreated (-EcN/-EcA; n = 6). EcN pretreatment completely abolished clinical signs of secretory diarrhea in +EcN/+EcA animals. Furthermore, jejunum epithelia of these animals did not exhibit an overshoot of secretory response upon stimulation with forskolin. Our studies demonstrate for the first time the efficacy of prophylactic EcN in pig small intestine for preventing an effect of toxigenic EcA. This infection model with freshly weaned piglets may be predestinated to further characterize EcN effects on the cellular level, i.e., involved second messenger pathways, or it may also be useful to examine the efficacy of other substrates or microbe strains against secretory stimuli.

CD4+ T cell mediated intestinal immunity: chronic inflammation versus immune regulation.

BACKGROUND: Several studies have suggested that chronic inflammatory bowel disease may be a consequence of antigen specific recognition by appropriate T cells which expand and induce immunopathology. AIMS: We wished to investigate whether autoreactive CD4+ T cells can initiate the disease on recognition of enterocyte specific antigens directly and if induction of mucosal tolerance occurs. METHODS: Transgenic mice (VILLIN-HA) were generated that showed specific expression of haemagglutinin from influenza virus A exclusively in enterocytes of the intestinal epithelium. To investigate the impact of enterocyte specific haemagglutinin expression in an autoimmune environment, we mated VILLIN-HA mice with T cell receptor (TCR)-HA mice expressing an alpha/beta-TCR, which recognises an MHC class II restricted epitope of haemagglutinin, and analysed the HA specific T cells for induction of autoimmunity or tolerance. RESULTS: In VILLIN-HAxTCR-HA mice, incomplete central deletion of HA specific lymphocytes occurred. Peripheral HA specific lymphocytes showed an activated phenotype and increased infiltration into the intestinal mucosa, but not into other organs of double transgenic mice. Enterocyte specific lamina propria lymphocytes showed a dose dependent proliferative response on antigen stimulation whereas the proliferative capacity of intraepithelial lymphocytes was reduced. Mucosal lymphocytes from VILLIN-HAxTCR-HA mice secreted lower amounts of interferon gamma and interleukin (IL)-2 but higher levels of tumour necrosis factor alpha, monocyte chemoattractant protein 1, and IL-6. Mucosal immune reactions were accompanied by broad changes in the gene expression profile with expression of proinflammatory genes, but strikingly also a remarkable set of genes discussed in the context of peripheral induction of regulatory T cells, including IL-10, Nrp-1, and Foxp3. CONCLUSIONS: Enterocyte specific antigen expression is sufficient to trigger a specific CD4+ T cell response leading to mucosal infiltration. In our model, progression to overt clinical disease was counteracted most likely by induction of regulatory T cells.