Non-necrotizing inflammatory granulomas (n-ngs) in the course of inflammatory bowel disease - immunology and clinical manifestation of intestinal and respiratory N-NGS.

OBJECTIVE: The aim:The article describes and summarizes the immunological pathomechanisms controlling the development of non-necrotizing granulomas in the course of non-specific inflammatory bowel diseases (IBD) in lungs and intestines; it also reviews the possible clinical correlations between the processes in the gastrointestinal and respiratory tracts based 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 cell subpopulation and macrophages predominate, producing IL-23. These are considered to be the key factors crucial for the occurrence of chronic inflammation. Another important causative 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 proteins similar to TNF-alpha. However, the interactions between gastrointestinal neuroendocrine peptides/amines (NEPA) and the immune system are believed to have a significant influence on the pathophysiology of non-specific inflammatory bowel diseases and non-necrotizing granulation. The key functions of the immune response of the gastrointestinal tract 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.