Thursday, July 16, 2015
Grand Hall and Gallery, Ground Floor & 1st Floor (Maritim Hotel)
Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic-relapsing disorder of the gastro-intestinal tract. Apart from genetic predisposition and environmental factors, an inappropriate immune response to the commensal flora is discussed as a major driving factor. Chemically-induced models reflect certain aspects of the disease very well, but their potential to study pathophysiology of IBD is limited. Our aim was to establish a model of bacteria-induced chronic gut inflammation to investigate the role of commensal versus pathogenic bacteria in the development of IBD.
C57BL/6 mice were infected with Salmonella enterica in combination with antibiotic treatment, resulting in a persistent infection and chronic inflammation in the gut. A clinical score was assessed and fecal bacterial load was evaluated systematically. Histological changes in colon tissue were assessed, and expression of inflammatory markers was analyzed in colon tissue sections and homogenates.
We observed a chronic infection in mice represented by a significantly elevated clinical score and persistent bacterial load in fecal pellets. Signs of chronic inflammation were also evident in sections of the colon tissue.
In summary, we propose a potential model of IBD that better reflects the natural etiology and the clinical features of the disease.
C57BL/6 mice were infected with Salmonella enterica in combination with antibiotic treatment, resulting in a persistent infection and chronic inflammation in the gut. A clinical score was assessed and fecal bacterial load was evaluated systematically. Histological changes in colon tissue were assessed, and expression of inflammatory markers was analyzed in colon tissue sections and homogenates.
We observed a chronic infection in mice represented by a significantly elevated clinical score and persistent bacterial load in fecal pellets. Signs of chronic inflammation were also evident in sections of the colon tissue.
In summary, we propose a potential model of IBD that better reflects the natural etiology and the clinical features of the disease.