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Biomedical subjects

R Louis

Publications and source records attributed to R Louis.

At least 73 records · Page 4Linked to original sources
PubMed1994

Potentiation of histamine release from human leucocytes by PAF.

Studies on the effects of PAF on histamine release from human leucocytes have yielded conflicting results. We therefore investigated the effects of PAF on leucocytic histamine release (HR) focusing on direct as well as on modulating effects. Peripheral blood leucocytes of normal and atopic subjects were incubated with PAF, anti-IgE and FMP for 30 min at 37 degrees C, and histamine was measured fluorometrically. Unlike anti-IgE (1/2000) and FMP (10(-5) M) which caused histamine release (HR) of 34 +/- 7% and 31 +/- 8%, respectively, PAF by itself (10(-11)-10(-5) M) failed to induce any significant HR from human leucocytes (< 3%) in normal (n = 14) and atopic subjects (n = 6). Nevertheless, in normals as well as atopics, PAF, but not lyso-PAF, enhanced anti-IgE (1/2000) and FMP (10(-5) M)-induced HR in a concentration-related manner. Maximal potentiation of histamine release caused by FMP and anti-IgE was achieved with PAF (10(-7)) (mean +/- SEM: 26 +/- 5%, n = 5, p < 0.01) and PAF (10(-5)) (mean +/- SEM: 20 +/- 7%, n = 7, p < 0.05), respectively. This potentiation was suppressed by WEB2086 (10(-5) M), a specific PAF antagonist. The time course of the enhancing effect produced by PAF was dependent on the type of secretagogue. The enhancement was nearly maximal when PAF and FMP were added simultaneously to the leucocytes, whereas a preincubation of 20 min with PAF was required to get maximal enhancement with anti-IgE. The enhancing activity of PAF on HR induced by both anti-IgE and FMP was reversed by washing the cells after preincubation. While PAF enhancement of FMP-induced HR persisted on mononuclear cell fraction containing basophils, that of anti-IgE-induced HR was considerably reduced under these conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

[Asthma and nonspecific bronchial hyperreactivity].

Bronchial hyperresponsiveness is a hallmark of asthma although it can also be present, to a lesser extent, in other diseases. The level of bronchial responsiveness depends on immuno-inflammatory processes modifying the functional status of airway smooth muscle as well as the structure of the bronchial wall. The responsiveness toward a direct constricting pharmacological agent is poorly correlated to the one toward an indirect constricting agent or a physical stimulus which cause airway obstruction through a more complex mechanism. Transversal studies show a relationship between the severity of asthma and the level of methacholine airway responsiveness. Long term treatment with corticoids can reduce the bronchial hyperresponsiveness of asthmatics.

Airway Obstruction↗
PubMed1994

Effects of acute injection of methylprednisolone in man on immunological and non-immunological histamine release from leucocytes and its potentiation by interleukin-3.

We investigated the effects of intravenous injection of methylprednisolone (MPR) compared with placebo (saline) on ex vivo leucocytic histamine release in eight healthy volunteers. All subjects received in a randomized and a single-blind manner the placebo and MPR, 20 mg and 125 mg, each injection given in 2 week intervals. On each occasion blood samples were taken just before and 24 h after the intravenous injection to determine circulating leucocyte counts and leucocytic histamine release induced by anti-IgE (1/2000) and FMP (Formyl-Methionyl-Phenylalanine) (10(-5) M) and its modulation by IL-3 (2 ng/ml). MPR 20 mg and 125 mg significantly increased circulating leucocyte counts (P < 0.05 and P < 0.001 respectively) but decreased leucocytic histamine content (P < 0.05 and P < 0.001 respectively) by 24 h. Placebo had no effect. As for circulating basophils, after 24 h they were decreased by 125 mg MPR (P < 0.05) but increased by 20 mg (P < 0.05). Anti-IgE-induced HR was significantly inhibited by 125 mg MPR (P < 0.05) but not by 20 mg MPR or by the placebo. In contrast, neither MPR (20 mg and 125 mg) nor placebo significantly reduced FMP-induced HR. The strong potentiation by IL-3 of HR evoked by anti-IgE and FMP at baseline (P < 0.001) persisted 24 h after injection of MPR or placebo (P < 0.001 except P < 0.05 for anti-IgE-induced HR after 125 mg MPR).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Decrease of T-lymphocyte proliferation in exercise-induced asthma.

The present study was designed to examine the effect of physical exercise on T-lymphocyte proliferation in patients with exercise-induced asthma (EIA). Indeed, a decrease in different immune functions is described in normal man after exercise. Thirty subjects (10 normal and 20 asthmatic subjects with or without EIA) underwent a submaximal exercise test on an electrically driven treadmill. Before and after this test, ventilatory variables were measured, and venous blood was taken to study plasma histamine (RIA) and spontaneous and phytohemagglutinin (PHA)-pulsed T-lymphocyte proliferation (mononuclear cells isolated on Ficoll-Hypaque; tritiated thymidine incorporation). Ten minutes after the end of the exercise, there was a significant FEV1 decrease only in asthmatic subjects with EIA (mean: 24 +/- 5%). In the same group, the mean plasma histamine level was 0.31 ng/ml-1 (+/- 0.06) before the challenge. It rose to 0.62 ng/ml-1 (+/- 0.14) 10 min after the end of the exercise (P < 0.05), and returned to normal limits 20 min after the test. In this group, there was also a significant decrease (by about 35%) of spontaneous and PHA-pulsed T-lymphocyte proliferation 2 and 4 h after the exercise. By contrast, exercise challenge had no effect on either plasma histamine level or T-lymphocyte proliferation in the normal group. Our results show a rapid and transient increase in plasma histamine in EIA. This was followed 2 and 4 h later by a significant decrease of T-lymphocyte proliferation. A possible relationship between these two phenomena is discussed.

Adolescent↗
PubMed1994

Cytokine modulation of basophil histamine release in wasp-venom allergy.

We report the effect of interleukin-3 (IL-3) and of other cytokines on antigen-induced basophil histamine release in wasp-venom-allergic subjects. Leukocytes from 12 patients with documented anaphylactic sensitivity to wasp venom were preincubated in the presence or absence of IL-3, granulocyte/macrophage-colony stimulating factor (GM-CSF), IL-5, IL-8, or stem cell factor (SCF). Washed cells were then exposed to venom and to other secretagogues, and histamine release in the supernatant was measured fluorometrically. Preincubation of leukocytes with IL-3, GM-CSF, or IL-5 (0.02-2 ng/ml), but not with IL-8 and SCF, caused a dose-dependent enhancement of antigen-induced basophilic histamine release in all subjects tested. Mean maximum increase was about 100% for IL-3, IL-5, and GM-CSF. The priming effect of IL-3 was rapid, persisted up to 12 h, and was not accompanied by a change in cellular histamine. IL-3 had a comparable enhancing effect when basophils were triggered with anti-IgE or N-formylmethionylphenylalanine (FMP). By contrast, IL-3 had no effect on substance-P-induced histamine release. The significant enhancement of basophil releasability to antigen in wasp-venom allergy by very low concentrations of IL-3, GM-CSF, and IL-5 suggests that cytokines in the basophil (mast-cell?) microenvironment could be critical factors in determining the variability of sting reactions in Hymenoptera-venom-allergic subjects.

Adolescent↗
PubMed1994

Modulation of immunological histamine release from human lung fragments by stem cell factor, IL-3, IL-5 and GM-CSF: comparison with human leukocytes.

Because of the importance of cytokines in the regulation of allergic inflammation, we investigated the effects of SCF, IL-3, IL-5 and GM-CSF on immunological histamine release from sensitized human lung fragments as well as human leukocytes. SCF (0.2-20 ng/ml) caused a concentration-related enhancement of anti-IgE (1/100) induced histamine release from lung fragments reaching maximally 64% at 20 ng/ml. In contrast, enhancement produced by IL-5, IL-3 and GM-CSF (0.2-20 ng/ml) was quite marginal and reached at best around 20% at the higher concentration, IL-5 being slightly more effective than IL-3 and GM-CSF. Further, SCF potentiated histamine release whatever the level of immunological control whereas potentiation by IL-5 primarily occurred when the amount of histamine release induced by the immunological control ranged between 5 and 10%. SCF acted synergistically with IL-5, producing a greater enhancement of histamine release than the sum of each cytokine used alone. Both SCF and, to a lesser extent, IL-5 potentiated anti-IgE-mediated histamine release regardless of passive sensitization of lung fragments. Unlike what was observed with lung fragments, IL-3, GM-CSF and to a lesser extent IL-5, were potent enhancing agents of anti-IgE (1/2,000)-induced histamine release from leukocytes. Maximal enhancement produced by IL-3 (20 ng/ml), GM-CSF (2 ng/ml) and IL-5 (20 ng/ml) reached 92%, 78% and 61%, respectively. By contrast, SCF (0.2-20 ng/ml) was ineffective on human leukocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Acute bronchial and hematologic effects following inhalation of a single dose of PAF. Comparison between asthmatics and normal subjects.

This study compared the acute bronchial and hematologic effects of inhaled platelet activating factor (PAF) (30 micrograms as a single dose) in 19 patients with mild asthma and 19 normal subjects. Each subject underwent a methacholine bronchial challenge 1 week before PAF challenge to determine the concentration of methacholine causing a 20 percent fall in FEV1 (PC20M). On the day of PAF challenge, specific conductance (SGaw), FEV1, FEF25-75, and platelet and leukocyte counts were measured before, and 5, 10, 15, and 20 min after PAF inhalation. Changes in pulmonary and hematologic parameters were expressed as percent of control (saline solution/ethanol solution). Unlike normal subjects, subjects with asthma had bronchial hyperresponsiveness to methacholine: geometric mean (range): 0.59 mg/ml (0.07 to 9.8) vs > 32 mg/ml. Acute bronchial obstruction over the first 20 min after PAF inhalation was more pronounced in asthmatics than in normal subjects whatever the functional index considered (p < 0.01). In asthmatics (n = 19), mean (SEM) maximal fall in SGaw, FEV1, and FEF25-75 reached 50 percent (6), 11 percent (4), and 19 percent (5), respectively, while in normal subjects (n = 19) the maximal decreases were 24 percent (6), 4 percent (1), and 6 percent (1), respectively. In asthmatics, no correlation was found between log PC20M and log fall in FEV1 after PAF (r = 0.04 p > 0.05). In asthmatics and normal subjects, inhaled PAF caused a transient fall in neutrophils and monocytes by 5 min followed by a full recovery at 15 min and 20 min. These hematologic changes were not significantly different between the two groups. While not correlated with their airway responsiveness to methacholine, asthmatics, compared with normal subjects, develop an exaggerated acute airway obstruction in response to PAF. In contrast, hematologic changes induced by PAF do not differ between asthmatics and normal subjects.

Administration, Inhalation↗
PubMed1993

Plasma histamine and bronchial reactivity in allergic asthma.

Histamine is an important mediator of allergic inflammation and bronchial hyperresponsiveness (BHR), a hallmark of asthma. Studies on the relationship between plasma histamine and BHR in allergic asthmatic patients have yielded controversial results. We therefore measured plasma histamine and bronchial reactivity in 30 nonsmoker volunteers taking no medication. Eleven were normal subjects; 19 were stable, mildly allergic asthmatic patients. Venous blood was taken to measure blood cells and basal plasma histamine by radioimmunoassay. After blood sampling, all subjects underwent a measurement of PC20M (concentration of methacholine causing a 20% fall in FEV1). Mean plasma histamine levels were 0.21 +/- 0.1 ng/ml and 0.44 +/- 0.3 ng/ml in normal and asthmatic subjects, respectively (P < 0.05). We found a significant increase of blood eosinophils and basophils in asthmatic patients, and a positive correlation between plasma histamine and circulating basophils. PC20M was greater than 16 mg in normal volunteers, and mean PC20M was 2.1 +/- 2 mg/ml in asthmatic patients. PC20M did not correlate with plasma histamine levels, but it did so negatively with blood eosinophils. The increased plasma histamine concentration in mildly atopic asthmatic patients might be a consequence of the high basophil releasability of atopics and the higher basophil counts in allergic asthma. Plasma histamine is thus unlikely to be a determinant of BHR in asthma.

Adolescent↗
PubMed1993

No increase in plasma histamine during PAF-induced airway obstruction in allergic asthmatics.

To investigate the possible role of mast cell or basophil histamine release in mediating platelet-activating factor (PAF) airway obstruction, we studied the effect of inhaled PAF (30 micrograms, single dose) on plasma histamine, bronchial caliber, and leukocyte and platelet counts in six patients with mild or moderate allergic asthma (mean age, 27 +/- 1.3 years; mean FEV1, 95 +/- 5 percent of predicted; mean PC20 methacholine, 1.46 +/- 0.36 mg/ml). Specific conductance (SGaw) FEV1, FEF25-75 percent, differential leukocyte and platelet counts, and plasma histamine (radioimmunoassay) were measured before and 5, 10, 15, and 20 min after PAF inhalation. Mean basal plasma histamine level was 0.28 +/- 0.04 ng/ml. Inhalation of PAF caused a fall in SGaw peaking at 5 min (43 +/- 9 percent) and a fall in FEV1 and FEF25-75 peaking at 10 min (19 +/- 10 percent and 30 +/- 13 percent, respectively). There was also a rapid and transient fall in circulating neutrophils at 5 min (from 3,096 +/- 204/mm3 to 2,551 +/- 158/mm3, p < 0.05) followed by a rebound neutrophilia. In contrast, plasma histamine level did not change significantly at any time measured. Conversely in the same asthmatics, a rapid rise in plasma histamine level (from 0.29 +/- 0.03 ng/ml at baseline to 0.53 +/- 0.06 ng/ml at 5 min; p < 0.01) was observed after an allergenic challenge (Dermatophagoides pteronyssinus) causing a fall in FEV1 peaking at 10 min (22 +/- 4 percent). Thus, inhaled PAF may induce airway obstruction and neutropenia in asthmatics without any significant change of plasma histamine level. These results indicate that it is unlikely that lung mast cells or basophils degranulate during PAF-induced bronchoconstriction.

Adult↗
PubMed1992

LY 186655, a phosphodiesterase inhibitor, inhibits histamine release from human basophils, lung and skin fragments.

LY 186655 (Tibenelast, Lilly) is a new phosphodiesterase inhibitor, not derived from the xanthine, possessing bronchodilating activity in animals. The aim of this work was to study the effect of LY 186655 and theophylline on histamine release from human leukocytes, skin and lung fragments. Histamine was measured using a spectrofluorometric method. Both drugs (3 x 10(-5)-3 x 10(-3) M) exhibited a dose-dependent inhibition on anti-IgE (1/2000)-induced histamine release from human leukocytes. At 3 x 10(-3) M, theophylline was significantly more effective than LY 186655 (mean inhibition 94 and 42%, respectively). On lung fragments, theophylline and LY 186655 (3 x 10(-5)-3 x 10(-3) M) caused strong and comparable inhibitory effects on anti-IgE (1/500)-induced histamine release with a mean inhibition reaching maximally 65%. Histamine release induced by compound 48/80 (1 mg/ml) on sliced human foreskin was reduced with both drugs (3 x 10(-3) M) by about 37%. We conclude that LY 186655 inhibits in vitro immunological histamine release from human lung and cutaneous mast cells as well as basophils with a similar pattern of activity to theophylline.

Adult↗