Biomedical subjects

W Boukhris

Publications and source records attributed to W Boukhris.

4 recordsLinked to original sources

PubMed1988

Differential effect of mixed D1/D2 and selective D2 dopaminergic antagonists on mouse T and B lymphocyte proliferation and interleukin production in vitro.

The effects of some dopaminergic antagonists were investigated on mouse lymphocyte proliferative responses in vitro. The mixed D1/D2 dopaminergic antagonists chlorpromazine, haloperidol and flupentixol inhibited 3H-Thymidine incorporation into adult BALB/c mouse spleen cells stimulated by concanavalin A, lipopolysaccharide from Escherichia coli, and allogenic cells in a mixed lymphocyte reaction. The inhibition was achieved at concentrations greater than 10(-6) M. It was not accounted for by decreased cell viability and it was no longer demonstrable when the compound was added 24 h or 48 h after the mitogenic stimulus. Conversely selective D2 dopaminergic antagonists sulpiride, metoclopramide and domperidone had no inhibitory effect at concentrations ranging from 10(-9) to 10(-5) or 10(-4) M. The three mixed D1/D2 antagonists inhibited the mitogenic effect of interleukin-1 on concanavalin A-stimulated thymocytes, but not the activity of interleukin-2 on the proliferation of the CTLL-2 cell line. The mixed D1/D2 antagonists interfered with the production of interleukin-2 but not with that of interleukin-1. These results indicate that dopaminergic antagonists may differentially affect lymphocyte proliferative responses to T or B cell mitogens or alloantigens. The mechanisms involved in terms of receptor specific or non specific phenomenons are discussed.

Animals↗

PubMed1987

Selective T cell defects induced by dopamine administration in mice.

Dopamine administration in BALB/c mice depressed the overall delayed-type hypersensitivity reaction to sheep red blood cells, the mixed-lymphocyte culture responses, the generation of cytotoxic T cells, and the number of spleen T cell populations. Conversely, dopamine enhanced concanavalin A stimulation of spleen cells, and had no effect on stimulation by PHA, on total spleen and thymus cell number, and on distribution of thymus Ly-t1+ or Ly-t2+ cell subsets. These results indicate that dopamine produces selective T cell defects probably mediated by a direct peripheral action of the drug on subsets of T lymphocytes.

Animals↗

PubMed1987

Impaired T-dependent immune response in L-dopa treated BALB/c mice.

Various neurotransmitters and neuropharmacological agents can affect lymphocyte responses. The purpose of the present study was to investigate the potential immunological effects of L-dihydroxyphenylalanine (L-dopa), the direct precursor of dopamine, by examining the influence of the in vivo administration of the drug on different functional and phenotypic parameters in BALB/c mice. L-dopa at the dose of 100 mg/kg/day altered T-dependent immune responses. The antibody response to sheep red blood cells (SRBC) was abolished by the drug. The delayed-type hypersensitivity reaction to SRBC was also depressed. Lymphocyte proliferation and generation of cytotoxic T cells in response to allogeneic stimulator cells in vitro were decreased by L-dopa treatment. These suppressive effects were correlated with a decrease in spleen T cells number. However, the proliferative response of spleen cells to concanavalin A was greatly enhanced by the L-dopa treatment. Conversely, there was no evidence for alteration of T-independent immune responses by L-dopa. Hence, the antibody response to TNP-Ficoll, and the proliferation of B spleen cells induced by E. coli lipopolysaccharide were unchanged. Altogether, these results showed that L-dopa which is converted to dopamine in the organism, could selectively affect T-dependent immune responses. The integration of these findings in the immune-neuroendocrine interactions, and the possible sites and mechanisms of action are discussed.

Animals↗

PubMedDate not supplied

Opposite effects of the catecholamines dopamine and norepinephrine on murine polyclonal B-cell activation.

The effects of dopamine (DA) and norepinephrine (NE) on polyclonal B-cell activation induced in vitro by lipopolysaccharide (LPS) and on cyclic AMP response in BALB/c mouse lymphocytes were investigated. DA at non-cytotoxic concentrations (5 x 10(-5) M and 10(-4) M) inhibited, but NE (5 x 10(-6) M to 5 x 10(-5) M) enhanced LPS-stimulated proliferation and Ig synthesis by lymphocytes from spleen, mesenteric lymph nodes and Peyer's patches. Depletion of adherent cells and T lymphocytes did not prevent the respective effects of DA and NE, and the drug effects were reproduced on nude (nu+/nu+) spleen cell proliferation and differentiation stimulated by LPS. The inhibitory effect of DA persisted even if the drug was added as late as 48 h after the mitogen. In contrast, NE was no longer stimulatory if added 2 h later than LPS. The effect of DA was blocked neither by DA1 or DA2 dopaminergic antagonists (SCH 23390 and sulpiride respectively), nor by alpha- or beta-adrenoceptor antagonists (phentolamine and propranolol respectively). Enhancement by NE was antagonized by propranolol, but not by phentolamine. Both DA and NE raised the level of cyclic AMP in unfractionated spleen cells as well as in B-enriched spleen cells but DA was less potent than NE. Pre-incubation of spleen lymphocytes with LPS for 1-24 h did not alter their cyclic AMP response to NE but it prevented the loss of sensitivity to DA after 4 or 24 h of in vitro incubation. The lysosomotropic agent chloroquine induced suppression of LPS-stimulated proliferation and Ig production with a dose-response profile similar to that of DA. Altogether, these results indicate that the catecholamines can exert opposite effects on polyclonal B-cell activation by acting directly on B lymphocytes.

Animals↗