Failure of Cytochalasin or Colchicine to inhibit Secretion of Immunoglobulins

SECRETIONS are often packaged in granules which are held within the cells of origin until some specific stimulus brings about release by exocytosis. Granules containing catecholamines are liberated from adrenal medullary cells by acetylcholine; granules containing insulin are released from pancreatic β-cells by high concentrations of glucose; and granules containing histamine, serotonin and slow-reacting substance are discharged from mast cells in the presence of cell-bound antibody and antigen. The release of secretory granules requires calcium ions in the extracellular medium¹ and may follow the entry into the cytoplasm of calcium ions which trigger contraction of an actomyosin-like microfilament system². This interpretation is supported by our recent observation² that induced release from mast cells of granules containing mediators of acute hypersensitivity is strongly inhibited by cytochalasins, a group of fungal products that selectively block the activity of microfilament-related contractile systems in many cells^3,4. Stimulated release of ¹³¹I from previously labelled mouse thyroids and endocytosis of colloid, are also inhibited by cytochalasin⁵. Cytochalasin inhibits cell movement, movement of ruffled membranes, pinocytosis and phagocytosis in macrophages and polymorphonuclear leucocytes^4,6. Release of ¹³¹ I from previously ¹³¹I-labelled mouse thyroid⁷ is also inhibited by colchicine and other agents that disperse labile cytoplasmic microtubules. Thus it seems that a contractile microfilament-related system, acting together with microtubules, brings about the controlled release, when required, of certain secretions.