ABSTRACT
Background: immune cells participate in the formation of atheromatous plate, however little is known about the effects of native or oxidatively modified lipoproteins on these cells. Aim: To study the effects of lipoproteins on in vitro mononuclear cell proliferation. Material and methods: peripheral blood mononuclear cells were obtained from 10 patients with type 2 diabetes mellitus (aged 52 ñ 9 years old with a disease duration of 8.2 ñ 5.7 years and a mean glycosilated hemoglobin of 9.3 ñ 2.2 percent) and 10 non diabetic healthy controls (aged 50.3 ñ 7.1 years old). These were stimulated with phytohemagglutinin (PHA) alone or in the presence of native LDLS, malondialdehyde modified LDLs or glycated LDLs. Proliferation was measured as 3H-thymidine incorporation and expressed as Stimulation Index (SI). Results: SI of patients and healthy subjects, after PHA stimulation were similar: (57.5 ñ 29.8 and 61.1 ñ 23.5) respectively LDLs did not induce proliferation in neither group. Native LDLs produced a 98 percent inhibition of PHA induced proliferation. Malondialdehyde modified and glycated LDLs caused a 50 percent inhibition. The suppressive effect was maintained when lipoproteins were incorporated to culture media 60 min prior or after PHA stimulation. Conclusions: Lipoproteins inhibit in vitro PHA induced peripheral blood mononuclear cell proliferation both in diabetic and in non diabetic subjects
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Diabetes Mellitus, Type 2/immunology , Immunosuppression Therapy , In Vitro Techniques , Lipoproteins, LDL/immunology , Phytohemagglutinins/pharmacology , Lymphoproliferative Disorders/immunology , Lymphocyte ActivationABSTRACT
Background: Advanced glycation end products are associated with chronic complications of diabetes mellitus. This glycation process renders many proteins immunogenic. Aim: To detect the presence of antibodies against albumin, collagen and low density lipoprotein glycation products in boys and teenagers with diabetes mellitus. Patients and methods : Thirty one patients with diabetes mellitus type I, aged 11ñ3.8 years and with a mean duration of disease of 3.7ñ2.7 years and 31 healthy controls aged 12.4ñ5.3 years were studied. Antibodies against glycation end products were detected by ELISA and results were expressed as a ratio of the optical density of the glycated protein/optical density of the native protein. Results : Diabetic patients and healthy controls did not have antibodies against albumin glycation end products. Diabetics had higher levels of antibodies than controls for collagen glycation end products (2.6ñ0.4 and 1.8ñ0.2 respectively, p< 0.01) and low density lipoprotein glycation end products (3.07ñ0.92 and 2.2ñ0.72 respectively, p< 0.05). Conclusions: The biological role of these antibodies is not clear. They could be a depuration mechanism for glycation end products or contribute to chronic complications of diabetes mellitus