NON–NECROTIZING INFLAMMATORY GRANULOMAS (N-NGS) IN THE COURSE OF INFLAMMATORY BOWEL DISEASE – IMMUNOLOGY AND CLINICAL MANIFESTATION OF INTESTINAL AND RESPIRATORY N-NGS

The aim:The article describes and summarizes the immunological pathomechanisms controlling the development of non-necrotizing granulomas in the course of non-specificinflammatory bowel diseases (IBD) in lungs and intestines; it also reviews the possible clinical correlations between the processes in the gastrointestinal and respiratory tractsbased on the example of Crohn’s disease (CD) and non-specific inflammatory bowel disease (IBC).While the dominant cell subpopulation in ulcerative colitis (UC) is Th2, which produces interleukins IL-4, IL-5, IL-6, IL-10 and IL-13 and Th17 cells; CD characterized by the Th1 cellsubpopulation and macrophages predominate, producing IL-23. These are considered to be the key factors crucial for the occurrence of chronic inflammation. Another importantcausative factor of non-specific inflammatory bowel diseases and granulation is the expression of CD40/CD40L proteins on activated T-cells, i.e. type 2 transmembrane proteinssimilar to TNF-alpha. However, the interactions between gastrointestinal neuroendocrine peptides/amines (NEPA) and the immune system are believed to have a significantinfluence on the pathophysiology of non-specific inflammatory bowel diseases and non-necrotizing granulation. The key functions of the immune response of the gastrointestinaltract are managed by the neuroendocrine regulatory system (NES) whose activities govern the production of various hormones including chromogranin/secretogranin, serotonin,vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), substance P, somatostatin or ghrelin.