In this study we have compared the adhesion of peripheral blood mononuclear cells (PBMC) to human umbilical vein endothelial cells (HUVEC) in a healthy control group with two groups of allergic asthmatics, not treated or treated with disodium cromoglycate (DSCG). The adhesion and blocking experiments were performed by the flow cytometric adhesion assay. No differences in the adhesion of lymphocytes were observed in any of the groups. The monocytes obtained from DSCG non-treated patients have shown significant (P<0.05) enhancement of adhesion to HUVEC in comparison to healthy controls. The treatment of asthmatic patients with DSCG downregulated the monocyte adhesion to cultured endothelial cells (ECs) and this was comparable to the group of normal donors. The DSCG may have a therapeutic effect on the regulation of monocyte adhesion in inflammatory and allergic diseases. The binding ability of untreated asthmatic PBMC to cultured ECs was partially inhibited by monoclonal antibody anti-CD54, suggesting that the increased EC adhesiveness for monocytes from allergic asthmatics may be at least partially dependent on the ICAM-1 adhesion pathways. Our results also indicate that the blocking agent anti-CD 18 was not essential for monocyte- endothelial interactions in allergic asthma.
Allergic processes are complex disorders in which inflammatory and immunological mechanisms are involved. Many studies indicate that the adhesion molecules are upregulated in allergic inflammation, and play a critical role in the pathogenesis of allergic inflammation. Modulation of the expression of adhesion molecules may provide a potential new target for therapeutic intervention in allergic diseases. In the present study the changes expression of adhesion molecules CDlla, CD18 (LFA-1), CD54 (ICAM-1) and L-selectin (CD62L) and VLA-4 (CD49d) were analysed by flow cytometry. Serum concentrations of soluble ICAM-1, VCAM-1 and soluble low affinity receptor for IgE concentrations sCD23 were measured by ELISA in atopic patients with mild asthma before and after treatment by disodium cromoglycate (DSCG). The most significant finding was a significant decrease of ICAM-1 expression on monocytes and CD49d on monocytes and lymphocytes as well as an increase of L-selectin expression on monocytes after treatment with DSCG, without any associated effect on CDlla and CD18. The levels of soluble ICAM-1 and VCAM-1 were not changed, only the levels of soluble CD23 that plays a regulatory role in ongoing IgE production, were decreased in asthmatic patients after the treatment with DSCG. These results suggest that DSCG diminishes cell activation.
We tested risperidone and ritanserin, serotonin-S2 receptor antagonists, for their effects on in vitro polyclonal IgG and IgM synthesis by human peripheral blood mononuclear cells (PBMC) stimulated with pokeweed mitogen (PWM). On the basis of the previously reported effect on immune function in vivo risperidone in this study was tested in three different groups of PBMC: healthy donors as well as schizophrenic patients before risperidone treatment and schizophrenic patients after the treatment with risperidone. IgG and IgM production after 7 days of culture was measured by ELISA. Risperidone decreased IgG synthesis (p<0.05) in PBMC of healthy subjects only at the highest concentration (10~6 M) and IgG synthesis enhanced by 5-HT was antagonized by risperidone. This effect, however, was not statistically significant. Neither risperidone nor ritanserin, in the concentration range 10-8- 10~6M, affected IgM synthesis in this group. Risperidone did not affect the production of IgG and IgM by PBMC of schizophrenic subjects in PWM-stimulated cultures both before and after risperidone therapy. The spontaneous production of IgG in PBMC of schizophrenic subjects before therapy was decreased (p<0.05) at concentrations 10-6-10~7 M of risperidone. We conclude that risperidone and ritanserin did not increase polyclonal IgG and IgM synthesis in vitro in contrast to neuroleptics currently used in clinical practice.