Inhibition of leukocyte migration after concanavalin A and phytohemagglutinin in patients with ulcers]

An attempt of the assessment of T-cells function in patients with gastric or duodenal ulcer has been undertaken. The studies involved 60 patients with gastric or duodenal ulcers and 47 individuals of the control group. Lymphocyte reactivity to different concentrations of concanavalin A and phytohemagglutinin has been assessed with leukocyte migration inhibition test. Lymphocyte T function has been examined also in patients with gastric or duodenal ulcers in reference to the theophylline-dependent and theophylline-sensitive subpopulation of T-cells. Leukocyte migration index values after phytohemagglutinin and concanavalin A did not differ significantly in patients with gastric or duodenal ulcers and theophylline-sensitive T-cells. Differences have been noted in the migration inhibition deficits. This phenomenon has been least frequent in case of phytohemagglutinin in the control group (5.8%) and most frequent in patients with gastric ulcer (62%). Percentage of patients responding to higher concanavalin A concentration (40 micrograms/ml) with leukocyte migration inhibition has been the highest in patients with duodenal ulcer. This index value has been significantly lower (p < 0.05) only in patients with duodenal ulcer and increased number of theophylline-dependent lymphocytes T. Increased reactivity of T-cells to higher concanavalin A concentration in patients with duodenal ulcer with theophylline-dependent T-cells in peripheral blood probably indicates increased the suppressor lymphocytes activity.     

Triiodothyronine affects the phytohemagglutinin to concanavalin A proliferative response ratio in sex-linked dwarf chickens

Euthyroid Cornell K strain and sex-linked dwarf (SLD) strain cockerels (which have abnormally low serum triiodothyronine concentrations) were supplemented with either 0, 0.01, 0.1, or 1.0 ppm of triiodothyronine (T3) in the diet. Peripheral blood lymphocytes (PBL) from these cockerels were obtained by slow-speed centrifugation (slow-spin-prepared PBL). The proliferative response of these PBL to phytohemagglutinin (PHA) and concanavalin A (Con A) was determined when the chicks were 6, 9, and 12 weeks of age. Con A responsiveness was also determined in 12-week-old cockerels using PBL which were separated on Ficoll (Ficoll-prepared PBL). Using slow-spin-prepared PBL, PHA, and Con A responsiveness increased in both strains with increasing levels of T3 supplementation. This enhancing effect of T3 was particularly evident in older cockerels. In 6- and 12-week-old SLD strain cockerels, the PHA:Con A response ratio was significantly (P less than 0.05) lower than in K strain cockerels. At 12 weeks of age the PHA:Con A response ratio of the SLD strain was elevated to K strain control levels by T3 supplementation. Therefore, the lower PHA:Con A response ratio in the SLD strain appears to be partially due to the existing peripheral hypothyroidism in this strain. Using Ficoll-prepared PBL, the effects of T3 on Con A responsiveness differed from those observed when slow-spin-prepared PBL were used. From this study we conclude that T3 supplementation affects mitogen responsiveness and the PHA:Con A response ratio. However, the effects of T3 on mitogen responsiveness depend on the age of the chicken, the level of T3 supplemented, the T cell population stimulated, and the method of lymphocyte enrichment.     

Lymphocyte commitment to DNA replication induced by concanavalin A

Commitment of lymphocytes to DNA replication induced by ConA was investigated by adding α-MM (a saccharide that competes with the lectin's lymphocyte binding sites) at various times to lymphocyte cultures that had been treated with a wide range of ConA concentrations. After 24 h of culture, α-MM addition has essentially no effect on cells treated with optimal concentrations of ConA, results in a marked blastogenic response of cells treated with supra-optimal (non-mitogenic) concentrations of ConA, and severely inhibits blastogenesis of cells treated with suboptimal concentrations of the lectin. Furthermore, the time of commitment is progressively shortened as the concentration of mitogen is increased. Thus, cells were committed to DNA replication as early as 5 h after incubation with supra-optimal concentrations of ConA. Induction of commitment does not occur when cells are incubated with ConA at 4 °C. Extensive crosslinking of membrane sites appears to be associated with the induction of early commitment by ConA, since the bivalent succinyl ConA failed to exhibit this effect. These findings indicate the need for re-evaluation of previous studies utilizing competing saccharides to determine kinetics of cell commitment to DNA replication.     

Lymphocyte response to phytohemagglutinin: Intracellular volume and intracellular [K+]

The effect of phytohemagglutinin (PHA) on lymphocytes was examined with respect to free intracellular water volume and intracellular [K⁺]. At a cell concentration of 30 × 10⁶ lymphocytes/ml in modified Hank's Buffered Salt Solution (HBSS) in the presence of 10% human AB serum, addition of PHA at 3 mg/ml resulted in a 24–27% decrease in free intracellular water space within 30 to 60 minutes and a return to control level after three hours. A larger change in intracellular water (44%) was observed under similar conditions in the absence of serum. The absolute intracellular K⁺ content did not change after PHA addition, but the cell water volume decrease arising from PHA addition resulted in a 29% increase in intracellular [K⁺] at 60 minutes. The decrease in lymphocyte water volume induced by PHA was also observed for concanavalin A which stimulates lymphocyte proliferation, but not for wheat germ lectin, an agglutinating agent which is not mitogenic. Thus, volume regulation may be closely associated with the mitogenicity of these compounds.     

Role of non-RT1 genes in the response of rat lymphocytes to Mycoplasma arthritidis T cell mitogen, concanavalin A and phytohemagglutinin

A comparison of splenic cells from various inbred rat strains indicated that DA, Lewis, Buffalo, August, Wistar Furth, and (LEW X BN)F1 all responded well to the Mycoplasma arthritidis T cell mitogen, phytohemagglutinin and concanavalin A, but cells from BN and MAXX rats were very weakly or nonresponsive. Cells from congenic strains expressing nonresponder background genes, and responder haplotypes at RT1 (BN.1L(LEW), RT1; BN.1A(DA), RT1av1) failed to respond significantly to the mitogens. Rats expressing responder background genes but the nonresponder haplotype at RT1 at RT1 (WF.1N-(MAXX), RT1n) exhibited high responses to all mitogens. The controlling role of non-RT1 genes was confirmed by testing tissue-typed (DA X BN)F2 progeny and (DA X BN)F1 X DA and (DA X BN)F1 X BN progeny. No association was seen between the expression of a/a, a/n, or n/n at RT1 and the degree of response to the mitogens. In contrast, as the proportion of DA non-RT1 genes increased, so did the degree of mitogenic responsiveness. Similar results were obtained by using a partially purified preparation of the mycoplasma T cell mitogen. The results indicated that in the (DA X BN)F1 hybrids, responsiveness to all mitogens was recessive: this contrasts with the (LEW X BN)F1 hybrids in which responsiveness was dominant. Finally, we showed that both responder and nonresponder splenic cells were capable of binding the M. arthritidis mitogen. The data contrast with those obtained with nonresponder mouse strains the cells of which failed to bind mitogen due to the absence of the E alpha chain of the I-E-coded molecule.     

Macrophages from human colostrum. Multinucleated giant cell formation by phytohemagglutinin and concanavalin A

Macrophages obtained from human colostrum were cultured in the presence of phytohemagglutinin (PHA), concanavalin A (Con A) and pokeweed mitogen (PWM). PHA caused multinucleated giant cell formation which could be inhibited by the addition of N-acetyl-d-galactosamine. Con A caused multinucleated giant cell formation and was cytotoxic in higher concentrations. Both effects could be inhibited by addition of α-methyl-d-mannoside and α-methyl-d-glucoside. PWM did not cause multinucleated giant cell formation but was cytotoxic in high concentrations.