PATHOGENESIS OF NON BACTERIAL CHRONIC PROSTATITIS

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Lymphocytes and lymphocyte-derived cytokines are thought to be critical in controlling chronic inflammatory processes by regulating the function of a wide variety of cells including inflammatory, immunologic and tissue cells (e.g. mast cells). Currently, little is known about the existence and role of T lymphocytes, mast cells, nerves and their products in non-bacterial chronic prostatitis (NBCP) and its associated chronic pain. Based on the growing body of literature on the role of lymphocyte-mast cell-nerve interactions in pain we have developed the following hypothesis: Hypothesis: Non-bacterial chronic prostatitis (NBCP), prostatodynia and chronic nonbacterial inflammation (CNBI) are inflammatory diseases of the prostate that result from an imbalance of specific T lymphocyte subpopulations (T1 vs. T2), which via their cytokine expression, regulate directly and indirectly the function of inflammatory, immunology and tissue cells (mast cells and nerves) within the prostate microenvironment, and thereby control both inflammation and pain within chronically inflamed prostate tissue. To test this hypothesis we propose the following goals: 1) to isolate, characterize and correlate T cells in fluids (blood, urine, prostate fluids) and tissue from NBCP, prostatodynia, CNBI and control patient populations. 2) to characterize and correlate the distribution of T1 and T2 cytokines in fluids and tissue from NBCP, prostatodynia, CNBI and control patients. 3) to characterize and correlate the distribution of mast cells and mast cell-related factors in NBCP, prostatodynia, CNBI and control patients. 4) to define the relationships between lymphocytes, mast cells and nerves in NBCP, prostatodynia, CNBI and control patients. 5) to quantify pain in patients with chronic prostatitis (NBCP, prostatodynia, and CNBI) using established validated instruments to correlate their clinical course with cell and cytokine results.