Acute non-specific inflammation and modification of macrophage and lymphocyte functions.
The acute inflammatory response is a common phenomenon experienced by the physician in a wide variety of clinical situations. One of the major problems facing the investigator in this field of research who wishes to look at the cellular and humoral responses involved, is that in most of the animal models previously used, the inflammatory reaction has been provoked in subcutaneous tissues. Thus, a quantitative assessment of leucocyte emigration and mediator production in the inflamed area is technically difficult without resorting to complicated and artificial methods. Inflammation provoked in the pleural cavity provides a useful tool in the study of these problems since the collection of cells and analysis of humoral factors in exudates is easily accomplished. Among the irritants that may be used, we focused our interest on calcium pyrophosphate (CaPP) crystals, a non-diffusible, non-antigenic and endotoxin-free irritant, because their deposition is implicated in pseudogout and chondrocalcinosis in man (MacCarty, 1973). Calcium pyrophosphate-induced pleurisy is typified by an acute reaction, dominated by polymorphonuclear leucocytes, reaching its maximal intensity at about 5 h and disappearing within 48 h (Willoughby et al., 1975). It was found to be independent of the complement system. Examination of the known mediators of inflammation revealed no significant participation of either histamine or 5-hydroxytryptamine. There was an early rise in PGE2 followed by a greater rise in PGF2 alpha as the reaction diminished (Capasso et al., 1975). More recently, we have demonstrated the presence of a small quantity of thromboxane and a large quantity of prostacyclin during the first 2 hours of this inflammatory process. It was also shown that this type of acute inflammation was accompanied by the very rapid liberation of acute phase proteins both locally, in the exudate, and systemically in the serum (Tissot et al., 1983). Some of these events were also examined during the pleural reaction to other types of irritants (Capasso et al., 1975) and gave similar results (Tissot et al., 1983).
D000818:Animals; D000917:Antibody Formation; D000920:Antibody-Dependent Cell Cytotoxicity; D002131:Calcium Pyrophosphate; D002177:Candidiasis / Q000276:immunology; D004247:DNA / Q000096:biosynthesis; D007375:Interleukin-1 / Q000096:biosynthesis; D007376:Interleukin-2 / Q000096:biosynthesis; D007710:Klebsiella Infections / Q000276:immunology; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000276:immunology*; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D010587:Phagocytosis; D010996:Pleural Effusion / Q000276:immunology; D010998:Pleurisy / Q000139:chemically induced / Q000276:immunology*; D051381:Rats; D014352:Trypanosomiasis / Q000276:immunology
D007375:Interleukin-1; D007376:Interleukin-2; D004247:DNA; D002131:Calcium Pyrophosphate