Effect of endogenous and synthetic sex steroids on the clearance of antibody-coated cells

Steroid hormones may influence the clinical expression of immunologic disease; however, their mechanism of action is uncertain. By using an experimental model, we studied the effect of sex steroids on the clearance of antibody-coated cells by macrophages in the spleen and liver. Progesterone significantly inhibited the clearance of IgG-coated E by splenic macrophages, whereas no effect was observed on the clearance of heat-altered E. This effect of progesterone was observed at serum concentrations which are attained during human pregnancy and the menstrual cycle. Furthermore, when splenic macrophages were isolated from progesterone-treated animals, they expressed decreased Fc gamma R activity. In addition, structural analogs of progesterone which have diminished glucocorticoid and progesterone activity retained this effect on macrophage Fc gamma R. In contrast, the estrogens estradiol and estriol as well as a structural estrogen analog with minimal estrogenic activity, 1,3,5(10)-estratrien-3,16 beta-diol, enhanced splenic macrophage Fc gamma R-dependent clearance. This action of estradiol could be partially inhibited by the antiestrogen tamoxifen. However, estradiol did not affect the C3-dependent clearance of IgM-coated E by hepatic macrophages. Concurrent administration of estradiol and progesterone demonstrated that the action of estradiol was predominant. These studies indicate that sex steroids alter splenic macrophage Fc gamma R function in vivo. This result may explain the alteration of disease activity in some human immunologic disorders during changes in hormonal state. Furthermore, analogs of progesterone and estrogen, as well as antiestrogens, which minimally affect the sex organs, retain the ability to alter splenic macrophage Fc gamma R function.     

Isolation and characterization of a new virus from owl monkeys: herpesvirus aotus type 3

Owl monkey kidney cell cultures yielded a viral agent 32 days after initiation of the culture. The virus was identified as a herpesvirus by physico-chemical, cultural, and morphological features. Serologically this herpesvirus was found to be unrelated to other members of this family, as well as to Herpesvirus aotus type 1 and 2. Based on these findings the name Herpesvirus aotus type 3 is suggested for this herpesvirus.     

Suppression of pulmonary and systemic vascular histamine H2-receptors in allergic sheep

We have previously demonstrated a depression of airway H2-receptor function in sheep allergic to Ascaris suum antigen. To investigate whether this is a generalized defect, we studied the H1- and H2- histamine receptor functions in the pulmonary and systemic circulations of allergic and nonallergic sheep. Pulmonary arterial pressure, and cardiac output were measured for calculation of pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR) before and immediately after a rapid intrapulmonary infusion of histamine (10 micrograms/kg), with and without pretreatment with H1- (chlorpheniramine) and H2- (metiamide) antagonists. Histamine alone increased mean PVR to 435 and 401% of base line and decreased mean SVR by 51 and 54% in the nonallergic and allergic sheep, respectively (P less than 0.001). In the nonallergic sheep following pretreatment with chlorpheniramine (selective H2 stimulation) or metiamide (selective H1 stimulation), histamine decreased SVR by 18 and 36%, respectively, suggesting that approximately two-thirds of the vasodepressor response was mediated by H1-receptors and one-third by H2-receptors. Combined H1- and H2-antagonists completely blocked the histamine response. In allergic sheep the histamine-induced decrease in SVR was primarily mediated by H1-receptors, because the response was blocked by H1-antagonist, chlorpheniramine, and the H2-antagonist, metiamide, had no effect. In the pulmonary circulation selective H1-stimulation caused a similar increase in PVR in allergic (365%) and nonallergic sheep (424%), whereas selective H2-stimulation caused a significant decrease in PVR in the nonallergic group (14%) but not in the allergic group.(ABSTRACT TRUNCATED AT 250 WORDS)