ABSTRACT
We investigated the effects of mixed leukocyte reaction (MLR), hydrocortisone (HC) and cyclosporine A (CsA) on the expression of leukocyte adhesion molecules on the mesangial (MC) and endothelial cells (EnC). Cell surface enzyme immunoassay showed that INFnu, IL-1beta, or TNF alpha stimulated expression of ICAM-1, or VCAM-1 on MC after 24 hours. Flow cytometric analysis demonstrated that MLR supernatant induced a marked increase in mean fluorescence of or % of cells highly expressing intercellular adhesion molecule(ICAM)-1 or vascular cell adhesion molecule (VCAM)-1 on both cells after 24 hours (p<0.001). HC treatment(300 ng/ml) during MLR effectively inhibited MLR-induced upregulation of ICAM-1 and VCAM-1 on both cells (p<0.005). When MLR supernatant with HC was added to adhesion molecule assay, there was no inhibitory effect of HC on VCAM-1. CsA treatment (500 ng/ml) during MLR caused a modest decrease in upregulation of VCAM-1 on EnC (p<0.05), but had no effects on ICAM-1 on both cells. CsA directly decreased expression of VCAM-1 on MC. In conclusion, alloreactive lymphocytes and monocytes upregulate the expression of VCAM-1 and ICAM-1 on target cells probably by the mediation of cytokines. HC effectively prevents MLR-induced upregulation of VCAM-1 and ICAM-1. CsA does not increase the expression of VCAM-1 and ICAM-1.
Subject(s)
Humans , Cells, Cultured , Cyclosporine/pharmacology , Endothelium, Vascular/drug effects , Glomerular Mesangium/drug effects , Hydrocortisone/pharmacology , Intercellular Adhesion Molecule-1/biosynthesis , Interleukin-1/pharmacology , Leukocytes/drug effects , Lymphocyte Culture Test, Mixed , Monocytes/drug effects , Tumor Necrosis Factor-alpha/pharmacology , Vascular Cell Adhesion Molecule-1/biosynthesisABSTRACT
We investigated the effects of mixed leukocyte reaction (MLR), hydrocortisone (HC) and cyclosporine A (CsA) on the expression of leukocyte adhesion molecules on the mesangial (MC) and endothelial cells (EnC). Cell surface enzyme immunoassay showed that INFnu, IL-1beta, or TNF alpha stimulated expression of ICAM-1, or VCAM-1 on MC after 24 hours. Flow cytometric analysis demonstrated that MLR supernatant induced a marked increase in mean fluorescence of or % of cells highly expressing intercellular adhesion molecule(ICAM)-1 or vascular cell adhesion molecule (VCAM)-1 on both cells after 24 hours (p<0.001). HC treatment(300 ng/ml) during MLR effectively inhibited MLR-induced upregulation of ICAM-1 and VCAM-1 on both cells (p<0.005). When MLR supernatant with HC was added to adhesion molecule assay, there was no inhibitory effect of HC on VCAM-1. CsA treatment (500 ng/ml) during MLR caused a modest decrease in upregulation of VCAM-1 on EnC (p<0.05), but had no effects on ICAM-1 on both cells. CsA directly decreased expression of VCAM-1 on MC. In conclusion, alloreactive lymphocytes and monocytes upregulate the expression of VCAM-1 and ICAM-1 on target cells probably by the mediation of cytokines. HC effectively prevents MLR-induced upregulation of VCAM-1 and ICAM-1. CsA does not increase the expression of VCAM-1 and ICAM-1.
Subject(s)
Humans , Cells, Cultured , Cyclosporine/pharmacology , Endothelium, Vascular/drug effects , Glomerular Mesangium/drug effects , Hydrocortisone/pharmacology , Intercellular Adhesion Molecule-1/biosynthesis , Interleukin-1/pharmacology , Leukocytes/drug effects , Lymphocyte Culture Test, Mixed , Monocytes/drug effects , Tumor Necrosis Factor-alpha/pharmacology , Vascular Cell Adhesion Molecule-1/biosynthesisABSTRACT
We studied 27 patients presenting with renal dysfunction after Stibamate therapy. Eighteen patients were proved cases of Kala Azar, others of PUO. Out of 10 cases in whom Kidney biopsy was done, 6 had tubular necrosis, one had mild mesangial proliferation and 3 had normal picture.