Document Type : Research Article
Bingol University, Veterinary Faculty, Microbiology Department, 12000 Bingol/TURKEY
Vocational School of Health Services, Department of Medical Services and Techniques, University of Bingol, 12000, Bingol
Department of Physiology, Hamidiye Faculty of Medicine, University of Health Sciences, 34000, Istanbul-Turkey
Department of Physiology, Faculty of Veterinary Medicine, University of Bingol, 12000, Bingol-Turkey;
Department of Histology and Embryology, Faculty of Veterinary Medicine, University of Bingol, 12000, Bingol-Turkey
Department of Animal Nutrition and Nutritional Diseases, Faculty of Veterinary Medicine, University of Bingol, 12000, Bingol-Turkey
Stress has been suggested to play an important role in the pathogenesis of gastric damage by either acting as a predisposing factor or a primary factor. Arcobacter species have frequently been isolated from stomach ulcer cases of pigs, but the role of these agents in the pathogenesis of the disease remains unclear.The primary aim of the present study was, to reveal the role of Arcobacter butzleri and stress in the etiology of gastric damage by establishing an experimental mouse design. Infection was induced by intra-gastric gavage of A. butzleri in two experimental groups comprising five weeks old specific pathogen-free (SPF) Balb/c mice. At 1, 2, 3, 4, and 7th weeks of the experiment, the animals were euthanized and examined for lesions occurring in the stomach. Histopathology, culture, and Polymerase Chain Reaction (PCR) were employed to detect development and severity of lesions and pathogens. In addition, serum corticosterone levels indicating the presence of stress in the mice were investigated by an ELISA method. Microscopic examination showed that the stomach of the experimental group had inflammatory reactions to varying degrees, but ulcers were not observed in the gastric mucosa of the animals exposed to A. butzleri and stress groups. The results suggested that A. butzleri and stress were predisposing factors in the formation of gastric ulcer, but failed to provide evidence for their causative role.