Divergent effects of methylxanthines and adenylate cyclase agonists on monocyte cytotoxicity and cyclic AMP levels.

The effects of theophylline, isobutylmethylxanthine (IBMX), prostaglandin E1 (PGE1), and isoproterenol on monocyte antibody-dependent cytotoxicity (ADCC) were compared with their effects on monocyte cyclic adenosine 3':5'-monophosphate (cAMP) levels. Theophylline (2 mmol/l) halved ADCC and gave a 2-fold increase in cAMP levels. At concentrations not elevating cAMP theophylline inhibited ADCC significantly.

Colchicine in generalized pustular psoriasis: clinical response and antibody-dependent cytotoxicity by monocytes and neutrophils.

Four patients with generalized pustular psoriasis were treated with oral colchicine in an open study. Three of the four patients went into total remission within two weeks while receiving colchicine. The monocyte- and neutrophil function was assessed by studying antibody-dependent cytotoxicity.

Enhanced monocyte and neutrophil cytotoxicity and normal cyclic nucleotide levels in severe psoriasis.

Eighteen patients with active psoriasis were investigated for antibody-dependent cell-mediated cytotoxicity (ADCC) mediated by monocytes and neutrophil leukocytes. Patients with extensive psoriatic lesions showed increased ADCC whereas patients with minimal psoriasis had normal monocyte and neutrophil function. After clinical remission the ADCC became normal.

Transient cyclic AMP accumulation during antibody-dependent cytotoxicity mediated by monocytes and neutrophils.

Monocyte and neutrophil cyclic nucleotide levels were recorded during antibody-dependent cell-mediated cytotoxicity (ADCC) mediated by monocytes and neutrophils. Addition of sensitized group A erythrocytes to monocytes and neutrophils and sensitized Rhesus D erythrocytes to monocytes gave a prompt one and a half to two-fold increase in cAMP levels (with maximal increases after 5–15 sec). No change in cGMP was obtained.

Histiocytosis X--an immune deficiency disease? Studies on antibody-dependent monocyte-mediated cytotoxicity.

Six children with histiocytosis X, all in clinical remission, were investigated for antibody-dependent cytotoxicity mediated by monocytes and neutrophils. Monocytes demonstrated a reduced cytotoxicity and a normal Fc receptor activity. Judged by light microscopy the monocytes were normal.

Dialyzable leukocyte extract stimulates cAMP in T gamma lymphocytes.

Dialyzable leukocyte extract (DLE) from human blood leukocytes gave a 3- to 8-fold increase in the cAMP concentration after addition to purified lymphocytes. No significant change in cGMP was observed. When purified lymphocytes were separated into T cells and non-T cells by an E-AET rosette technique the cAMP response was most pronounced in T cells.

Antibody-dependent monocyte-mediated cytotoxicity in atopic dermatitis. Relation to clinical state and cyclic AMP response.

Antibody-dependent monocyte-mediated cytotoxicity was investigated in adult patients with atopic dermatitis. In patients with active dermatitis monocyte cytotoxicity was reduced. Serial studies of individual patients demonstrated that a reduced cytotoxicity in clinical exacerbation did not normalize during clinical remission.

Oral disodium cromoglycate in mastocytosis.

Oral disodium cromoglycate was found useful for the treatment of gastrointestinal manifestations of mastocytosis in 2 patients with systemic disease. The urinary excretion of histamine in these 2 patients decreased following treatment. Oral disodium cromoglycate had no effect on cutaneous symptoms, either in these 2 patients nor in 2 other patients with urticaria pigmentosa without signs of systemic mastocytosis.

Impaired monocyte cyclic AMP responses and monocyte cytotoxicity in atopic dermatitis.

Purified monocytes from 21 patients with mild and severe atopic dermatitis (AD) were compared with 22 healthy controls with respect to antibody-dependent cell-mediated cytotoxicity (ADCC) and cyclic adenosine 3',5'-monophosphate (cAMP) responses to stimulatory agents. ADCC was depressed in both severe and mild atopic dermatitis. The patients showed decreased cAMP responses to isoproterenol and histamine, the decrement being more distinct in severe atopic dermatitis.

Antibody-dependent monocyte-mediated cytotoxicity. The interference by platelets, immune complexes, and normal serum.

Monocyte mediated lysis of human type B-erythrocytes coated with heat-inactivated anti-B serum was measured as 51Cr-release. Preincubation of monocytes with heat-inactivated normal AB serum inhibited cytolysis while a strong stimulation of cytolysis was seen with fresh AB serum. These effects of serum were reversible upon cell washing.

Impaired monocyte-mediated cytotoxicity in atopic dermatitis.

Twenty-three adult patients with atopic dermatitis of different severity and extent all without present cutaneous infection were investigated for antibody-dependent cytotoxicity mediated by purified monocytes. Compared to a healthy control group the monocyte cytotoxicity was significantly decreased for patients with more widespread dermatitis. Eight patients with acute contact dermatitis and 13 patients with extrinsic asthma or allergic rhinitis showed normal cytotoxicity.

The role of calcium and cyclic adenosine 3',5'-monophosphate in the regulation of glycogen metabolism in phagocytozing human polymorphonuclear leukocytes.

Incubation of human polymorphonuclear leukocytes in a glucose-free Krebs-Ringer bicarbonate buffer for 2 h resulted in glycogen depletion, decreased phosphorylase activity and increased synthase-R activity. Addition of dialyzed latex particles to starved leukocytes revealed a very rapid ingestion rate (half-maximal ingestion within 30 s). This uptake is followed by glycogenolysis associated with an immediate two-fold increase in phosphorylase a activity and a synthase-R to -D conversion within 30 s.

Effects of catecholamines and glucagon on glycogen metabolism in human polymorphonuclear leukocytes.

Addition of 10 micron of the alpha-adrenergic agonist phenylephrine to polymorphonuclear leukocytes suspended in glucose-free Krebs-Ringer bicarbonate buffer (pH 6.7) activated phosphorylase, inactivated glycogen synthase R maximally within 30 s, and resulted in glycogen breakdown. Phenylephrine increased 45Ca efflux relative to control of 45Ca prelabelled cells, but did not affect cyclic adenosine 3',5'-monophosphate (cAMP) concentration.