THE RÔLE OF INFLAMMATION IN IMMUNITY

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Abstract
The princi-pal sequences in the development of inflammation may be listed as follows: "Increased fluid passage through the capillary endothelial wall. This seems to be primarily referable to two factors: 1. Elevation in capillary pressure which is perhaps the outcome of a local axon reflex affecting the caliber of arterioles. 2. Increased capillary permeability; this seems to be referable to the liberation by injured tissue of the permeability factor tentatively termed leukotaxine. Leukotaxine is a crystalline nitrogenous substance, the significant properties of which evidently do not resemble those of histamine. It appears to belong to the group of relatively simple polypeptides. It is postulated that its formation occurs as a result of the presence of an irritant interfering with local protein catabolism. In localization of the irritant (fixation) the ''walling-off'' of an inflamed area seems to be due to an enhanced passage of fibrinogen through the more permeable capillary wall. The mechanism of fixation is primarily referable to the formation of a fibrinous network and of thrombi occluding the lumina of draining lymphatics. This favors the development of lymphatic blockade in acute inflammation. Various secondary factors, such as the presence of immune bodies in anaphylactic or allergic inflammation, may reinforce the basic mechanism. The early occurrence of fixation in a severely injured area plays a definite role in immunity, for it allows an interval in which the relatively sluggish leukocytes may assemble for the purpose of phagocytosis. Migration of leukocytes. The first cells to migrate into an inflamed area are the polymorphonuclear leukocytes. The mechanism of their migration seems to be related to the liberation of leukotaxine by injured tissue. The properties of the crystalline nitrogenous substance recovered from exudates offer a reasonable explanation for two of the basic sequences of the inflammatory reaction: first, the initial increase in capillary permeability, and secondly, the rapid emigration of polymorphonuclear leukocytes into injured tissue. Leukotaxine appears to contain factors concerned both with permeability and chemotaxis. The polymorphonuclear cells are gradually displaced by macrophages. Cytological changes in acute inflammation seem to be conditioned by the pH of the exudate which in turn is frequently referable to disturbance in the local intermediary carbohydrate metabolism. The development of a local acidosis, resulting from increased glycolysis and depletion of the alkali reserve, seems to injure the polymorphonuclear cells. Macrophages survive and predominate when the pH falls to a level of about 6.9 or 6.8. Further reduction in the pH proves lethal to all types of leukocytes and frank suppuration ensues. The role of lymphocytes or of plasma cells in certain types of inflammation remains to be elucidated. The interplay and dynamic relationships of the above sequences constitute an acute inflammation. The inflammatory reaction thus displays an extraordinary complex mechanism tending to localize and dispose of a chemical or bacterial irritant. This ultimately leads to organization and repair of the affected tissue. The concept of fixation and its mechanism affords a rational interpretation of the role of inflammation in immunity. The capacity of patho-genic microorganisms to disseminate from their site of inoculation is apparently inversely related to the intensity of induced local injury. In this way inflammation plays a significant role in problems of immunity as a regulator of bacterial invasiveness.".