What are the chemical mediators in the inflammatory response?
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THIS BRIEF review will cover only some of the important aspects of the subject but will try to define an outline from which one can gain a reasonable concept of current knowledge and proceed to further detailed investigation if he desires. One is also directed to recent detailed reviews1-3 which should be of considerable interest. From the time of the original stimulus (heat, ultraviolet, toxins, antigens, trauma, etc) to the restitution of normal function there is a very complicated, and for the most part unknown, series of humoral and cellular events described by the ancient term, inflammation. A mediator may be defined as an endogenous chemical agent which takes an active part in the development of the inflammatory response. We are then concerned primarily with chemical (mediator) agents which are associated with and responsible for the events occurring during inflammation. Exogenous agents which induce inflammatory responses are not
Both divinyl benzene copolymer (plastic) beads and schistosome eggs produce inflammatory reactions after intravenous deposition into the lung of a mouse. As reported previously, the schistosome egg granuloma is an immunologic reaction of the delayed hypersensitivity type; this inflammatory process is prevented by immunosuppressive measures, and characteristically demonstrates an anamnestic response. In contradistinction, the plastic bead granuloma appears to be characteristic of a foreign body reaction; it is unaffected by immunosuppressive measures and does not demonstrate an anamnestic response with repeated exposure. The data in this report suggest that the granuloma formation around plastic beads is a nonimmunologic reaction induced by chemical mediators of inflammation. This proposal is supported by the following findings: the plastic beads activate Hageman factor in normal human and mouse plasma; the plastic beads induce vascular permeability-enhancing activity as measured in guinea pig skin and kinin-like activity in normal human and mouse plasma that is dependent on Hageman factor; ellagic acid, an agent that activates Hageman factor in vivo and is reported to diminish kininogen by consumptive depletion, markedly depresses the plastic bead granuloma. These data are consistent with the idea that the plastic bead granuloma and perhaps other foreign body inflammatory reactions are in major part dependent on kinin formation. Ellagic acid also suppressed the schistosome egg granuloma, but not to the same degree as the plastic bead granuloma. The implications of this observation are discussed in the text. Silicosis and "blue velvet disease", pathologic processes associated with the deposition of silica and magnesium trisilicate, respectively, in the lung, and the induction of a foreign body reaction may also be dependent on the activation of chemical mediators of inflammation by the silica and magnesium trisilicate particles with immunologic mechanisms participating in only a minor way, if at all. The marked suppression of experimental silicosis and blue velvet disease in mice by ellagic acid supports this idea.
What are the 5 inflammatory responses?There are five fundamental signs of inflammation that include: heat (calor), redness (rubor), swelling (tumor), pain (dolor), and loss of function (functio laesa).
What is the role of chemical mediators in acute inflammation?Chemical mediators of inflammation
These substances can act via direct stimulation of cell surface receptors (e.g. histamine) or function as plasma derived factors that cause direct tissue damage (e.g. complement).
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