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Biomedical subjects

A R Rabson

Publications and source records attributed to A R Rabson.

At least 91 records · Page 5Linked to original sources
PubMed1977

The in vitro effects of histamine and metiamide on neutrophil motility and their relationship to intracellular cyclic nucleotide levels.

Histamine at concentrations of 1 x 10(-5) M to 5 x 10(-5) M consistently increased neutrophil movement as measured in Boyden chambers. This effect was entirely caused by stimulation of chemokinesis (stimulated random migration) and true chemotaxis was inhibited by these concentrations. This inhibition of chemotaxis could be abolished by pretreatment with metiamide, an H-2 receptor antagonist, and levamisole, but not by diphenylhydramine, an H-1 receptor antagonist. Metiamide at similar concentrations produced a mild stimulation of chemokinesis but has no effect on true chemotaxis. The histamine effects on neutrophil motility were associated with increased levels of intracellular cAMP wehreas cAMP levels were unaffected. Agents known to elevate intracellular cAMP levels produced effects on neutrophil motility similar to those of histamine. It is suggested that histamine exerts a 2-fold effect on neutrophil motility mediated via an H-2 receptor site and associated with elevated levels of cAMP.

Cell Movement↗
PubMed1977

The effect of PHA-activated MN-cell supernatants on polymorphonuclear leucocyte function.

The effect of PHA-activated mononuclear-cell (MN) supernatants on various polymorphonuclear-leucocyte (PMN) functions were assessed. Treatment of PMN with PHA-activated MN-cell supernatants resulted in greater electrophoretic mobility, indicating an increase in the negative surface charge. PMN directional motility was inhibited in the presence of active supernatants but was not affected by a pulse exposure of the PMN to these supernatants. Neither control nor active supernatants were chemotactic for PMN, but treatment of these cells with active supernatants produced an increase in their phagocytic activity, their ability to reduce NBT and in their glucose oxidation through the hexosemonophosphate shunt. Bactericidal capacity of these PMN was unaltered. Specific loss of leucocyte inhibitory factor (LIF) activity from supernatants of PHA-activated MN cells followed their absorption with PMN cells but not with human MN cells or guinea-pig peritoneal exudate cells. Furthermore, acquired inhibition of migration of the absorbing PMN was observed.

Blood Bactericidal Activity↗
PubMed1977

An inhibitor of lymphocyte proliferation and lymphokine production released by unstimulated foetal monocytes.

Supernatants obtained from 3-day cultures of cord blood monocytes inhibited normal lymphocyte activation by either PHA or in a two-way MLC. Both lymphocyte transformation and lymphokine production was significantly inhibited by these supernatants but not by those derived from adult mononuclear cell cultures. The inhibitory material produced by foetal monocytes was dialysable and was non-cytotoxic to target cells. It is postulated that this factor contributes to the depressed maternal cell-mediated immune response observed in pregnancy.

Female↗
PubMed1976

Defective leucocyte inhibitory factor (LIF) production by lymphocytes in children with kwashiorkor.

Production of the lymphokine leucocyte inhibitory factor (LIF) by phytohaemagglutinin (PHA)-stimulated lymphocytes was assessed in 25 children with kwashiorkor. Although the lymphocytes of 12 of these patients produced adequate amounts of LIF, the rest of the group failed to produce lymphokine after PHA activation. There was no correlation between the ability to produce LIF and the age, severity of malnutrition or any other clinical parameters assessed in these patients. This finding confirms the presence of defective cell-mediated immunity observed in a substantial proportion of kwashiorkor children.

Humans↗
PubMed1976

Production of leucocyte migration inhibitory factor by neonatal lymphocytes.

Lymphocytes (mononuclear cells) from cord blood of 10 normal placentas and from 10 normal adults were assessed for production of leucocyte migration inhibiting factor (LIF) after phytohaemagglutinin (PHA) stimulation, as a measure of cell-mediated immunity. Mononuclear cells from both adult and cord blood produced adequate quantities of LIF, indicating that neonatal lymphocytes have the ability to manufacture normal amounts of lymphokines.

Adult↗
PubMed1976

The blocking by autologous serum of maternal cell-mediated immune reactions to placental antigen.

The reactivity of splenic lymphocytes to a placental antigen was assessed in pregnant and control rats by means of a macrophage migration inhibition test. The pregnant but not the control animals, showed increasing cell-mediated immunity, which persisted until the second week after parturition. Migration inhibition could be abolished when sensitised lymphocytes were first pulsed with serum from the pregnant animal in the presence of antigen. This blocking effect was obtained only with autologous but not with normal or heterologous pregnant rat serum, and did not occur when antigen was omitted from the pulse. The results indicate that pregnant animals have cell-mediated immunity against a placental antigen, but the serum of these animals has a central enhancing effect which is antigen-dependent.

Animals↗
PubMed1976

Deficiency of adenosine deaminase not associated with severe combined immunodeficiency.

The 12-year-old Kung (""Bushman'') boy from South West Africa who has marked deficiency of red cell adenosine deaminase has been found to have 2 to 3% of enzyme activity in red blood cells, 10 to 12% in leukocytes, and 10 to 30% in cultured fibroblasts. The enzyme has ADA 1 electrophoretic mobility: SV40 transformation of cultured fibroblasts caused a decrease of ""tissue ADA'' and an increase in ""red cell ADA'' isozymes. A battery of investigations revealed that the child has normal humoral and cellular immunity. A family study showed that a sibling had the same level of red cell ADA and the parents had intermediate levels. Studies of the Kung population from which the child comes have shown that the allele responsible for the condition, and which we designate ADA8, is polymorphic.

Adenosine Deaminase↗
PubMed1976

Defective neutrophil motility in children with measles.

The random migration and chemotactic ability of neutrophils from ten patients with uncomplicated measles was found to be grossly impaired when compared to a group of normal children. Chemotaxis to endotoxin activated serum and to hydrolysed casein was markedly depressed, but serum from measles patients, when activated by endotoxin, generated and chemotactic activity and did not contain leukotactic inhibitors. The defect in neutrophil motility was confirmed in vivo by abnormal Rebuck skin windows. The defect was temporary, and recovery of normal chemotaxis was observed by the eleventh day after the onset of the rash.

Cell Movement↗
PubMed1976

Homozygous human C3 deficiency. The role of C3 in antibody production, C-1s-induced vasopermeability, and cobra venom-induced passive hemolysis.

Studies of the family of a patient with marked deficiency of the third component of complement (C3) demonstrated that the patient was homozygous for a blank allele at the C3 locus, C3-. Metabolic studies with purified radiolabeled C3 in the patient revealed a mildly elevated fractional catabolic rate and a markedly reduced synthesis rate, consistent with a lack of C3 synthesis as the patient's primary defect. There was also a mild increase in the rate of conversion of purified C3 added to her serum and incubated at 37 degrees C in vitro. Major blood group-compatible erythrocytes from a patient with paroxysmal nocturnal hemoglobinuria had the same shortened survival in the C3-deficient patient as in a normal control. Although no leukocytosis developed in the patient in spontaneous infection by pyogenic organisms, there was a normal leukocytosis in response to the injection of thyphoid vaccine. The intradermal injection of C-1s, which produces a marked increase in vasopermeability in the skin of normal subjects, produced no definite change in the patient, possibly implicating C3 or a protein in the alternative pathway as the normal mediator of this response. The patient's serum exhibited near-normal immune adherence activity, confirming the lack of requirement of C3 for this function. C5 inactivation and passive hemolysis of unsensitized guinea pig erythrocytes occurred normally in C3-deficient serum on incubation with cobra venom factor, indicating that C3 is not required for these reactions. The patient's humoral antibody response to both protein and carbohydrate antigens was entirely normal, making it unlikely that C3 is required for antigen processing.

Alleles↗
PubMed1976

The effects of cyclic AMP on leucocyte inhibitory factor (LIF) production and on the inhibition of leucocyte migration.

The effect of drugs known to increase intracellular levels of cyllic AMP were studied in the leucocyte migration ihibition system. It was found that cyclic AMP, dibutyryl cyclic AMP, theophyline, and prostaglandins E1 and E2 inhibited the production of leucocyte inhibiting factor by HA pulsed lymphocytes Inhibition only occured when the drugs were present during or after the PHA pulse. In addition it was found that these drugs enhanced the migration of polymorphonuclear leucocytes (PMN), in this system. Electrophoretic mobility of PMN cells was not altered by these drug indicating that the effect is not due to changes in membrane charge. However, granulocyte adhesion was reduced in the presence of these drug suggesting that adhesion is of primary importance in the migration of polymorphonuclear leucocytes out of capillary tubes. The findings show that cyclic AMP is important in modulating both cell-mediated and inflammatory responses.

Bucladesine↗
PubMed1976

In vitro stimulation of neutrophil motility by levamisole: maintenance of cgmp levels in chemotactically stimulated levamisole-treated neutrophils.

Levamisole at concentrations of 10(-3) M or 10(-4) M consistently increased neutrophil random motility and chemokinesis (stimulated random migration). Similar concentrations also increased directional movement of polymorphonuclear leukocytes to both endotoxin-activated serum and hydrolyzed casein. This effect on chemotaxis was due to a true stimulation and was not due solely to increased random movement. The effect of levamisole on the neutrophils could be removed by washing, but persisted if the cells were initially treated with levamisole and serum or endotoxin-activated serum. After neutrophil stimulation with chemotactic factor an initial rise in intracellular cyclic AMP levels was detected which was not influenced by prior levamisole treatment. Intracellular cyclic GMP levels after an initial slight depression, returned to resting levels and gradually diminished over a 60-minute period. Levamisole-treated cells consistently showed higher cyclic GMP levels and it is postulated that by maintaining intracellular cyclic GMP levels, microtubular assembly and cell motility might be enhanced.

Caseins↗
PubMed1976

Leucocyte capillary migration: an adherence dependent phenomenon.

To determine the mode of action of leucocyte inhibitory factor (LIF) on polymorphonuclear leucocyte (PMN) migration out of capillary tubes, this phenomenon has been compared with PMN adhesion to cotton wool columns. Colchicine and vinblastine sulphate had no effect on either of these processes but cytochalasin B caused marked inhibition of PMN migration and increased PMN adhesion. The cytochalasin B effect could be reversed in the presence of drugs known to increase intracellular levels of cyclic AMP. For inhibition of PMN migration by LIF, Mg2+ but not Ca2+ was essential. LIF not only inhibited PMN migration but also increased PMN adhesion to cotton wool columns. LIF inhibitory activity on PMN migration was not affected by colchicine or vinblastine. Leucocyte migration and adhesion depend on similar mechanisms, and are both influenced by LIF which probably acts by affecting micro-filament function.

Calcium↗
PubMed1976

Polymorphonuclear leucocyte function in chronic renal failure and after renal transplantation.

Neutrophil chemotaxis, phagocytosis and bactericidal ability were assessed in patients with chronic renal failure on conservative therapy, in others on regular peritoneal and haemodialysis, and in a group of patients who had received renal allografts. Chemotaxis was abnormal in all groups. The groups on peritoneal and haemodialysis had mildly impaired phagocytosis, while killing ability was normal in all but the group on conservative therapy who showed a mild defect. Serum from groups when activated with endotoxin was poorly chemotactic to normal neutrophils, but functioned normally as opsonins for phagocytosis.

Blood Bactericidal Activity↗
PubMed1976

Depressed neutrophil chemotaxis in patients with chronic renal failure and after renal transplantation.

Polymorphonuclear leukocyte chemotaxis, phagocytosis, and bactericidal ability were tested with neutrophlis from patients with chronic renal failure on conservative therapy, from others of regular peritoneal dialysis or hemodialysis, and from a group of patients who had received renal allografts. Chemotaxis was depressed in all groups. Phagocytosis was mildly impaired in the two groups on dialysis. The leukocytes of patients on conservative therapy had mildly decreased killing ability, whereas this function was normal in other groups tested. Sera from all patients, when activated with endotoxin, were poorly chemotactic to normal neutrophils, especially in those on conservative therapy and hemodialysis, but these sera functioned normally as opsonins for phagocytosis. The observed defect in chemotaxis could account, at least partly, for the frequency of bacterial infections in these patients.

Bacteriolysis↗
PubMed1976

In vitro reversal of cellular unresponsiveness induced by levamisole.

Mononuclear cells from twenty-one patients with depressed cellular reactivity were assessed for the ability to produce leucocyte inhibitory factor (LIF) and to transform after PHA stimulation, in the presence or absence of levamisole. Cells from nineteen patients failed to produce significant lymphokines when stimulated with PHA alone, but after a prior 1-hr levamisole pulse normal amounts of LIF were produced. Unstimulated mononuclear cell supernatants from six patients showed LIF-like activity, which could be abolished or decreased in five of the six when the cells were initially treated with levamisole. Mononuclear cells from seven of twelve patients which failed to incorporate [3H]thymidine after PHA activation, showed an increased response after a 1-hr levamisole pulse. Unstimulated mononuclear supernatants from six patients inhibited the lymphoproliferative response of normal cells to PHA. After treatment with levamisole, however, the suppressive effect of these supernatants was decreased or abolished. In vitro levamisole treatment, therefore, not only restores cellular responsiveness in anergic patients but also restricts the uncontrolled release of inhibitory factors.

Cells, Cultured↗
PubMed1975

Generalized Yersinia enterocolitica infection.

The clinical course of generalized Yersinia enterocolitica infection in 13 patients was observed. Two syndromes were apparent; seven patients had an acute septicemic picture, whereas the rest had a subacute localizing infection that usually produced hepatic or splenic abscesses. The latter form often resembled amebic hepatitis clinically, and five of the six patients died despite antibiotic treatment. The acute septicemic form of the disease resembled systemic salmonellosis, and most cases responded to therapy with the appropriate antibiotics.

Abscess↗