Prostaglandins and the Acute Phase Immune Response

Abstract

The acute phase of the immune response occurs in response to infectious agents. This initial phase occurs within minutes of the challenge which results in a cascade of immune interactions and the most prominent and easily measured manifestation of this immunostimulation is fever. Experimentally the acute phase response, especially fever, can be induced in animals by administering the purified components of the infectious agents which stimulate this response. The purified component of bacterial cell walls, endotoxin (lipopolysaccharide, LPS), can mimic the immunological activation observed during infection and can be used to determine immune responsiveness. Similarly it is possible to mimic the immunoactivation observed during viral infection by using synthetic agents which are similar to viral components and in this respect the synthetic double-stranded ribonucleic acid polyinosinic: polycytidylic acid (poly I:C) has been extremely useful. Fever and the acute phase in general occur in a series of steps in response to the sequential production of mediators within the body. The initial challenge leads to the induction and release of interleukin-1 (IL-1) [1] which is synthesised by various cells in the body especially peripheral blood monocytes or tissue macrophages. IL-1 concomitantly inducethe production of prostaglandins from many cells, if not all, in the body and this increase in the level of prostaglandins [1], specifically prostaglandin E2, (PGE2) is responsible for ultimately producing a febrile response (Fig. 1).