Biomedical subjects

M P Maldague

Publications and source records attributed to M P Maldague.

3 recordsLinked to original sources

PubMed1988

Increase in the number and the phagocytic function of guinea pig pulmonary and peritoneal macrophages following oral administration of RU 41740, a glycoprotein extract from Klebsiella pneumoniae.

RU 41740 (Biostim) which is a purified glycoprotein extract from Klebsiella pneumoniae, is an orally active non-specific immunostimulant. In guinea pigs, 8 days after a 7 days oral administration of RU 41740 (10 or 100 mg/kg/day), an increase in the cell population of the pulmonary and peritoneal cavities was observed, especially in that of the macrophages. RU 41740 also enhanced the phagocytic activity of both the alveolar and peritoneal macrophages, when their chemotactic activity was not significantly modified. This increase in the number of pulmonary macrophages and the stimulation of their phagocytic function might explain the protective effect afforded by the oral administration of Biostim against respiratory infections in patients with chronic bronchitis.

Administration, Oral↗

PubMed1982

Increased complement-mediated leukocytic histamine release in atopics.

Complement-mediated leukocytic histamine release was compared in normal and atopic subjects using isolated leukocytes or heparinized blood. Leukocytes were treated with zymosan-activated autologous serum, whereas blood was directly incubated with zymosan particles. Histamine released from basophils into the leukocyte supernatant or plasma was measured spectrofluorometrically and expressed in percent of total histamine. In atopics, the mean histamine release (47% for leukocytes and 12% for blood) was significantly higher than in normals (30% and 5%, respectively). Individual variations were large in both groups, and a good concordance was noted between the two techniques. By cross-experiments using activated isologous serum from AB donors instead of autologous serum, it was demonstrated that individual variability was not due to differences in intensity of complement activation. Passive sensitization of normal leukocytes with IgE antibodies increased their ability to release histamine in the presence of activated serum. Thus, high complement-mediated leukocytic histamine release is more commonly found in atopics, and appears to be secondary to an intrinsic abnormality of basophils. It is suggested that complement activation and subsequent inflammation could play, especially in house dust-caused asthma, a more important role than previously appreciated. Moreover, an exaggerated mediator releasability as may occur even in nonatopic subjects, could possibly explain some predisposition to interstitial pulmonary diseases caused by inhalants capable of activating complement.

Adult↗

PubMed1981

Depression of neutrophil chemotaxis in atopic individuals. An H2 histamine receptor response.

Neutrophil chemotaxis was compared in normal and atopic individuals using a modified Boyden chamber with as chemotactant, autologous serum either unactivated or activated by zymosan or an endotoxin-containing house dust preparation. A high incidence of defective leukotaxis was found in atopics when cells were opposed to activated serum. The cause of this abnormality is not intrinsic to the leukocytes since random migration and chemotaxis towards unactivated serum were comparable in normal and atopic subjects. The defect persisted when atopic leukocytes were opposed to activated normal serum and the chemotactic response of normal neutrophils was not imparied when tested against activated atopic serum. Leukotaxis was significantly depressed by incubating atopic leukocytes with allergen to which they were sensitized, suggesting an inhibitory effect of mediators of anaphylaxis. Histamine inhibited in vitro neutrophil chemotaxis in normal and atopic subjects. This inhibition was dose-related and significantly more pronounced in atopics. Incubation of atopic leukocytes with an H2 antagonist, cimetidine, was capable of enhancing their chemotactic responsiveness towards activated autologous serum to levels observed in normal controls. In the same conditions, an H1 blocker, promethazine, was without effect. These data indicate that the leukotactic dysfunction of atopic individuals results from an abnormal sensitivity of these leukocytes to histamine which, in the chemotactic chamber, may be released from basophils by products of complement activation and, in some experimental conditions, by antigen to which cells are sensitized.

Chemotaxis, Leukocyte↗