Prostaglandins and granuloma formation in vivo.
The formation of granuloma tissue is one of the major characteristics of chronic inflammation. Infiltration of phagocytic cells (a major source of prostaglandins) and in many cases (including rheumatoid arthritis) lymphocytes, is one of the earliest events in granuloma formation. Prostaglandins (PGs) may modulate the infiltration of some or all of these cells, though much in-vivo data is lacking. Additionally, PGs may modulate the release of the products of these inflammatory cells, which contribute to granuloma formation. Once granulomatous tissue becomes established, PGs may also control the growth of the granuloma through actions on proliferating cells and connective tissue constituents. In-vivo data suggest that the anti-granuloma actions may be mediated by cyclic AMP. While prevention of endogenous PG production by anti-inflammatory drugs has little beneficial effect on preexisting granuloma, facilitation or mimickry of the anti-granuloma actions of PGs may be a possible line for future therapy of diseases such as rheumatoid arthritis.
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000503:physiopathology; D003238:Connective Tissue / Q000503:physiopathology; D004195:Disease Models, Animal; D005347:Fibroblasts / Q000502:physiology; D006099:Granuloma / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D008264:Macrophages / Q000502:physiology; D009504:Neutrophils / Q000502:physiology; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000494:pharmacology / Q000502:physiology; D011817:Rabbits
D011453:Prostaglandins; D011458:Prostaglandins E