DISEASE PROCESSES IN SEASTARS: A METCHNIKOVIAN CHALLENGE

¹ Department of Pathobiology, The Johns Hopkins University, School of Hygiene and Public Health, Baltimore, Maryland 21205, and, Marine Biological Laboratory. Woods Hole, Massachusetts 02543.

The adult seastar is an ideal model for study of phagocytosis and inflammation. The behavior of the circulating amebocytes responsible for phagocytosis and clumping can be directly observed in the coelomic fluid circulating in the transparent papulae of the limbs. Intracoelomic injection of an autologous amebocyte extract induces temporary, reversible, clumping and adherence of amebocytes. Injected, foreign, red-pigmented sea urchin amebocytes are phagocytosed by seastar amebocytes which then form clumps in the tips of the papulae and traverse to the external surface through penetrating lesions. Successive injections may cause acute inflammation and edema. During the acute inflammatory response, a substance(s) is released into the coelomic fluid which stimulates the urn cell complex of Sipunculus nudus to secrete mucus in vitro; the substance disappears from the fluid by 24 hours. A spontaneous ciliate infection of seastar testes causes failure of the infected animal's amebocytes to clump on glass or plastic. Seastars recognize foreign grafts, but the role of amebocytes in the rejection has not been shown to be explicit. In the separate water vascular system of seastars, a secondary inflammatory response (amebocyte clumping) is induced by injections of bacterial suspensions and by repeated injection of sea urchin amebocytes into the coelom. Heavy exposure of seastars to ciliate populations induces appearance of a lysin which is not derived from circulating cells.