Nickel challenge up regulates CD69 expression on T lymphocyte sub-sets from patients with nickel induced contact dermatitis

Background: Persistent antigenic stimulation due to repeated exposure to nickel may lead to chronic inflammation resulting in allergic contact dermatitis (ACD).Objectives: This study was performed to assess nickel induced immune activation among patients sensitized against nickel.Patients and Methods: A total of 35 patients (29 females and 6 males; mean age 36±9 years) with nickel contact dermatitis and 20 patch test negative healthy individuals  (14 females and 6 males; mean age 29±7 years) were included in this study. Peripheral blood of patients and controls was incubated with nickel sulfate for 24 hours. Immune activation was assessed by CD69 up-reg- ulation on T lymphocyte sub-sets by flow cytometry.Results: Base line expression of CD69 on CD8+ lymphocytes was higher among patients compared to controls (4.1±1.3%vs2.8±1.1%;p<0.009). There was no difference in proportions of CD±CD69+ cells between patients and controls (3.2±0.9%vs2.3±0.8%). Exposure to nickel induced expression of CD69 on a significantly higher proportion of CD4+ lympho- cytes (22.1±6.2%) of the ACD patients compared to controls (2.8±2.5%;p<0.0001). Similarly nickel induced CD69 expression on a higher proportion of CD8+ lymphocytes (18.2±5.3%) from ACD patients compared to the controls (1.9±1.8%;p<0.0006).Conclusion: CD69 molecule appears to be an important regulator of immune response in nickel contact dermatitis.   Keywords: Nickel, CD4+, CD8+, CD69, contact dermatitis

Nickel challenge up regulates CD69 expression on T lymphocyte sub-sets from patients with nickel induced contact dermatitis

Background: Persistent antigenic stimulation due to repeated exposure to nickel may lead to chronic inflammation resulting in allergic contact dermatitis (ACD). Objectives: This study was performed to assess nickel induced immune activation among patients sensitized against nickel. Patients and Methods: A total of 35 patients (29 females and 6 males; mean age 36\ub19 years) with nickel contact dermatitis and 20 patch test negative healthy individuals (14 females and 6 males; mean age 29\ub17 years) were included in this study. Peripheral blood of patients and controls was incubated with nickel sulfate for 24 hours. Immune activation was assessed by CD69 up-regulation on T lymphocyte sub-sets by flow cytometry. Results: Base line expression of CD69 on CD8+ lymphocytes was higher among patients compared to controls (4.1\ub11.3%vs2.8\ub11.1%;p<0.009). There was no difference in proportions of CD\ub1CD69+ cells between patients and controls (3.2\ub10.9%vs2.3\ub10.8%). Exposure to nickel induced expression of CD69 on a significantly higher proportion of CD4+ lymphocytes (22.1\ub16.2%) of the ACD patients compared to controls (2.8\ub12.5%;p<0.0001). Similarly nickel induced CD69 expression on a higher proportion of CD8+ lymphocytes (18.2\ub15.3%) from ACD patients compared to the controls (1.9\ub11.8%;p<0.0006). Conclusion: CD69 molecule appears to be an important regulator of immune response in nickel contact dermatitis. DOI: https://dx.doi.org/10.4314/ahs.v19i1.19 Cite as: Zahid S, Mustafa A, Dina A, Sawsan B, Felwa A, Mohammed G, et al. Nickel challenge up regulates CD69 expression on T lymphocyte sub-sets from patients with nickel induced contact dermatitis. Afri Health Sci. 2019;19(1). 1460-1466. https://dx.doi. org/10.4314/ahs.v19i1.1

Suppression of type 2 diabetes mellitus-induced aortic ultrastructural alterations in rats by insulin:an association of vascular injury biomarkers

Diabetes represents a major public health problem and an estimated 70% of people with diabetes die of cardiovascular complications. The protective effect of insulin treatment against ultrastructural damage to the tunica intima and tunica media of the aorta induced by type 2 diabetes mellitus (T2DM) has not been investigated before using transmission electron microscopy (TEM). Therefore, we induced T2DM in rats using high fat diet and streptozotocin (50 mg/kg) and administered insulin daily by i.v injection for 8 weeks to the treatment group. Whereas, the T2DM control group were left untreated for the duration of the experiment. A comparison was also made between the effect of insulin on aortic tissue and the blood level of biomarkers of vascular injury, inflammation, and oxidative stress. T2DM induced profound ultrastructural damage to the aortic endothelium and vascular smooth muscle cells, which were substantially protected with insulin. Furthermore, insulin returned blood sugar to a control level and significantly (p &lt; .05) inhibited diabetic up-regulation of endothelial and leukocyte intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion protein 1 (VCAM-1), endothelial cell adhesion molecules, P-selectin and E-selectin, tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), and malondialdehyde (MDA). Furthermore, insulin augmented the blood level of the anti-oxidant enzyme superoxide dismutase (SOD). We conclude that in a rat model of T2DM, insulin treatment substantially reduces aortic injury secondary to T2DM for a period of 8 weeks, possibly due to the inhibition of hyperglycemia, vascular activation, inflammation, and oxidative stress.</p

Suppression of type 2 diabetes mellitus-induced aortic ultrastructural alterations in rats by insulin:an association of vascular injury biomarkers

Diabetes represents a major public health problem and an estimated 70% of people with diabetes die of cardiovascular complications. The protective effect of insulin treatment against ultrastructural damage to the tunica intima and tunica media of the aorta induced by type 2 diabetes mellitus (T2DM) has not been investigated before using transmission electron microscopy (TEM). Therefore, we induced T2DM in rats using high fat diet and streptozotocin (50 mg/kg) and administered insulin daily by i.v injection for 8 weeks to the treatment group. Whereas, the T2DM control group were left untreated for the duration of the experiment. A comparison was also made between the effect of insulin on aortic tissue and the blood level of biomarkers of vascular injury, inflammation, and oxidative stress. T2DM induced profound ultrastructural damage to the aortic endothelium and vascular smooth muscle cells, which were substantially protected with insulin. Furthermore, insulin returned blood sugar to a control level and significantly (p &lt; .05) inhibited diabetic up-regulation of endothelial and leukocyte intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion protein 1 (VCAM-1), endothelial cell adhesion molecules, P-selectin and E-selectin, tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), and malondialdehyde (MDA). Furthermore, insulin augmented the blood level of the anti-oxidant enzyme superoxide dismutase (SOD). We conclude that in a rat model of T2DM, insulin treatment substantially reduces aortic injury secondary to T2DM for a period of 8 weeks, possibly due to the inhibition of hyperglycemia, vascular activation, inflammation, and oxidative stress.</p