Blood mononuclear cells mobilization and cytokines secretion during prolonged exercises.

This study was designed to compare the effects of three prolonged exercises varying in their intensity and duration, on blood mononuclear cell mobilization and cytokine secretion (IL1(1)-IL(2)). Seven healthy subjects underwent three effort trials (45 % VO(2)max during 4 h - 60% VO(2)max during 3 h - 75 % VO(2)max during 2 h) at one-month intervals. Blood samples were drawn before, different times during exercise and also after exercise. Prolonged exercises induced a transient increase in blood mononuclear cells which occurred across all intensity levels. We also observed a significant increase in plasma IL(1) level during exercise which correlates with the exercise intensity. The mean IL(1) level increased up to 2.5 times after the three proposed exercises (p <0.05). Plasma IL(2) level decreased at the end of prolonged exercises irrespective of the exercise intensity. No correlation was observed between blood mononuclear count and cytokine determination. Our data suggest that blood mononuclear cells mobilization is associated but not correlated with alterations of cytokine levels.

Effect of prolonged exercise on neutrophil myeloperoxidase secretion.

This study was designed to compare the effects of three prolonged exercises on plasma myeloperoxidase concentrations, used as marker of neutrophil degranulation. Seven healthy subjects underwent three effort trials (45% VO2max during 4 h, 60% VO2max during 3 h, 75% VO2max during 2 h) at one-month intervals. Blood samples were collected before, during and after exercise. Myeloperoxidase levels were measured by radioimmunoassay. We observed a significant increase in myeloperoxidase concentration (+85%) at the end of our three prolonged exercises (p < 0.05). This myeloperoxidase increase was not correlated with the modification of neutrophil count, suggesting that neutrophil degranulation is independent of their mobilisation.

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.

Histamine-induced inhibition of neutrophil chemotaxis and T-lymphocyte proliferation in man.

Histamine inhibits in vitro human neutrophil chemotaxis and T-lymphocyte proliferation via H2 receptors. The aim of this study was to verify these inhibitory effects of histamine in man in vivo. Healthy volunteers were challenged with histamine by intravenous (1 mg), subcutaneous (1 mg) and inhalatory (2.4 mg) routes. Venous blood was taken before and at different times after challenge. Neutrophil chemotaxis was studied by the Boyden assay and T-lymphocyte proliferation by counting H3-thymidine incorporation in cultured mononuclear cells. Plasma histamine was measured by radioimmunoassay. Histamine infusion caused transient systemic symptoms as well as a significant decrease of neutrophil chemotaxis (mean - 26% +/- 6) and of PHA-pulsed T-lymphocyte proliferation (mean - 16% +/- 6) 4 h after histamine challenge. Subcutaneous injection of histamine caused only a significant decrease of neutrophil chemotaxis (mean - 24% +/- 15) 4 h after injection. Histamine inhalation was well tolerated and caused a significant depression of neutrophil chemotaxis (mean - 40% +/- 15) and of T-lymphocyte proliferation (mean - 27% +/- 6) 2 and 4 h after the challenge. Histamine challenges were always accompanied by a rapid and transient rise in plasma histamine. Inhalation of an H2 agonist (impromidine) but not of an H1 agonist (betahistine) caused a decrease of neutrophil chemotaxis and of T-lymphocyte proliferation. Oral pretreatment with an H2 antagonist (cimetidine) before histamine inhalation prevented histamine-induced decrease of neutrophil chemotaxis and T-lymphocyte proliferation, whereas astemizole, an H1 antagonist, had no effect. In conclusion, during the few hours following administration, exogenous histamine in man causes a depression of neutrophil chemotaxis and T-lymphocyte proliferation via H2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Depression of polymorphonuclear chemotaxis and T-lymphocyte proliferation following histamine inhalation in man.

Histamine, in vitro, via H2-receptor activation, exerts an inhibitory effect on polymorphonuclear (PMN) chemotaxis and T-lymphocyte proliferation. The aim of this study was to verify these histamine inhibitory effects in man. Healthy and asymptomatic asthmatic volunteers inhaled a histamine (0.1%), methacholine (0.1%) or saline aerosol for 3 min. Asthmatics were selected on the basis of low bronchial sensitivity to pharmacological agents. Blood was taken before and at different times following aerosol challenge. PMN chemotaxis was studied in vitro by the Boyden assay. T-lymphocyte proliferation was measured by counting H3-thymidine incorporation in cultured mononuclear cells. Plasma histamine was measured by a specific and sensitive radioimmunoassay. Inhalation of histamine or methacholine caused a 22-43% decrease in forced expiratory volume in one second (FEV1) in asthmatics only. In both groups, there was a transient increase of plasma histamine immediately following histamine inhalation, and 2 and 4 h later, a significant decrease of PMN chemotaxis and T-lymphocyte proliferation. Inhalation of methacholine or saline had no effect on leukocytes. Oral administration of an H2-receptor antagonist, cimetidine, before histamine inhalation, prevented the decrease of PMN chemotaxis and T-lymphocyte proliferation, whereas astemizole, an H1-antagonist, had no effect. In conclusion, histamine, at a dose commonly used for bronchial provocation tests, causes, in man, 2 and 4 h after inhalation, a depression of PMN chemotaxis (tested in vitro) and T-lymphocyte proliferation through activation of H2-receptors.