It has recently been demonstrated by three independent research groups including ours that interleukin 1 (IL-1), a polypeptide hormone produced by activated monocytes or macrophages, or both, stimulates the release of hypothalamic corticotropin-releasing factor (CRF). Since CRF acts centrally in the brain to reduce food intake, we hypothesized that IL-1 might induce anorexia through this central action of CRF. The present study was carried out to examine the hypothesis, using male Wistar rats. Based on three lines of evidence, we report here that IL-1, both endogenously released and exogenously administered, induces the suppression of food intake in rats and that endogenous CRF in the brain is involved in the IL-1-induced anorexia. First, lipopolysaccharide (LPS), a potent stimulant of the release and production of endogenous IL-1, caused anorexia in a dose-related manner, and this effect was significantly blocked by pretreatment with glucocorticoid hormones, which have been shown to inhibit the production of endogenous IL-1 by LPS. Second, intraperitoneal injection of IL-1 resulted in a dose-related suppression of food intake. Third, anorexia induced by IL-1 was diminished by the immunoneutralization of endogenous CRF in the brain. These results provide further evidence of the existence of bidirectional communication between the immune and neuroendocrine systems. Furthermore, this connection between IL-1 and CRF may represent a mechanism by which anorexia results from the activation of the immune system by such immunological challenges as acute infectious diseases.

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The bone marrow of a 53-year-old woman with acute myeloid leukemia (AML) with disseminated intravascular coagulation was investigated by transmission electron microscopy. The patient had a preceding granulocytic sarcoma, and subclinical disseminated intravascular coagulation occurred concomitantly with the development of AML. Ultrastructural findings of the bone marrow at the onset of AML revealed the following: (1) The cytoplasm of the leukemic cells showed frequent fragmentation, resulting in the formation of abundant cytoplasmic fragments. (2) These cytoplasmic fragments were surrounded by abundant fibrin fibers, forming the fibrin-cytoplasmic fragment complex (FCF complex). (3) Slight fibrin deposition was seen around the leukemic cells and in the intercellular space of the bone marrow. Fibrin deposition in the bone marrow is thought to represent morphologic evidence of disseminated intravascular coagulation. The damage on the leukemic cell surface due to the cytoplasmic fragmentation seems to be closely related to the development of disseminated intravascular coagulation.