0000000000365461
AUTHOR
Daniel Seidel
Isolation and subsequent analysis of murine lamina propria mononuclear cells from colonic tissue
Studies on colonic cells in the lamina propria (LP) of mice are important for understanding the cellular and immune responses in the gut, especially in inflammatory bowel diseases (such as morbus crohn and colitis ulcerosa). This protocol details a method to isolate LP cells and characterize freshly isolated cells by quality control experiments to obtain cells that can be used for further investigations. After different steps of digestion of the tissue using collagenase, DNase and dispase, the resulting cells are purified using Percoll gradient. The success of the isolation can be analyzed by cell viability test (Trypan Blue exclusion test) and by flow cytometric analysis to assess apoptosi…
Perforin deficiency attenuates inflammation and tumor growth in colitis-associated cancer
Background: Patients with inflammatory bowel disease (IBD) have a markedly increased risk to develop colon cancer, but there are only limited data about the host antitumor response in such colitis-associated cancer. In the present study we aimed at assessing the role of perforin-dependent effector mechanisms in the immune response in a murine model of colitis-associated colon cancer. Methods: Wildtype and perforin-deficient mice were analyzed in a mouse model of colitis-associated colon cancer using azoxymethane (AOM) and dextran sodium sulfate (DSS). Results: Tumors of wildtype mice showed infiltration of CD4+, CD8+ T cells, natural killer (NK) cells, high numbers of apoptotic cells, and e…
949 IDENTIFICATION OF TWO CLINICALLY DISTINCT SUBTYPES IN AUTOIMMUNE HEPATITIS BY COMPARATIVE FUNCTIONAL GENOMICS
Conclusion: Incidence of autoimmune hepatitis is increasing, as other autoimmune diseases in developed countries. The main recognised hypothesis is the ‘hygienist theory’ (improvement of hygien leading to a decrease in infections) with few putative non exclusive mechanisms involving antigenic competition, extension of immune regulation induced by exogenous bacterial antigen or Toll Like Receptors.