Interferon-gamma, immunoglobulin-E and vascular endothelial growth factor in children with papular urticaria

Papular urticaria [PU] is a common childhood disorder. It is a chronic allergic disease caused by insect bites. Both immediate and delayed type hypersensitivity reactions could be involved in the pathogenesis of PU. The immediate reaction is responsible for the immunoglobulin-E [IgE] response supported by T-helper 2 [Th2] cells while the delayed reaction is mediated by Thl cytokines particularly interferon-gamma [IFN-alpha]. Mast cells which are effector cells of IgE-mediated immune responses, can release vascular endothelial growth factor [VEGF] after IgE-dependant activation. VEGF was reported to play a role in the pathogenesis of many allergic conditions. This study included 28 children with papular urticaria and 15 age and sex-matched healthy controls. The age of the patients ranged from 2 to 7 years [mean, 3.5 years]. The duration of PU ranged from 3 months to 4 years. IFN-alpha, IgE and VEGF levels were quantitatively determined in serum of patients and controls by Enzyme Linked Immuno-Sorbent Assays [ELISA]. Children with papular urticaria showed significantly elevated serum levels of IFN-alpha, IgE and VEGF compared to healthy controls [p<0.05, p<0.001 and p<0.001 respectively]. A significant positive correlation was demonstrated between serum levels of IFN-y and IgE in children with papular urticaria [r-= 0.941, p<0.01]. Papular urticaria could be mediated by a complex immune response involving more than one mechanism, with evidence for both Thl response [increased production of IFN-alpha] and Th2 response [increased production of IgE] with a possible role for VEGF

Tissue levels of Interleukin-1 Beta are positively correlated with nitric oxide in patients with Generalized Vitiligo

Recent studies indicated that interleukin-1 beta [IL-1beta] enhance the activity of nitric oxide [NO] synthase resulting in release of excess amounts of NO. The later has been implicated in the pathogenesis of vitiligo. The objective of this study was to determine the correlations between levels of IL-1beta and NO in both tissues and sera from patients with generalized vitiligo. Our study included 30 patients with generalized vitiligo and 15 normal controls. Tissue and serum levels of IL-1 beta and NO were measured using enzyme immunoassay and a spectrophotometer, respectively. Tissue and serum levels of NO were significantly higher in patients with generalized vitiligo than controls [0.58 +/- 0.19 vs 0.41 +/- 0.17 and 58.05 +/- 12.19 vs 28.82 +/- 3.98; p <0.01 and p <0.001; respectively]. Tissue and serum levels of IL-1 beta in patients with generalized vitiligo were significantly higher than controls [4.86 +/- 1.94 vs 2.18 +/- 0.71 and 22.09 +/- 2.64 vs 15.34 +/- 3.55; p <0.001 and p<0.001; respectively]. A significant positive correlation was found between tissue levels of NO and IL-1 beta [r = 0.82, p <0.001]. Tissue levels of IL-1 beta were significantly correlated with extent of vitiligo [r = 0.57, p <0.01]. Patients with generalized vitiligo had significantly increased tissue and serum levels of NO and IL-1 beta. Tissue levels of IL-1 beta were positively correlated with tissue levels of NO, and extent of vitiligo

Melatonin and N-acetyl cystein protect rats against carbon tetrachloride-induced acute liver damage

The present study was designed to investigate the protective effects of melatonin [MLT] and/or N-acetylcystein [NAC] against carbon tetrachloride [CCl4] induced liver cirrhosis in rats. Injection of CCl4 [2 ml/kg] to adult female wistar rats produced a significant elevations in alanine transaminase [ALT], aspartate transaminase [AST], serum and liver Malonaldehyde [MDA] and serum nitric oxide [NO]. The maximal percentages of increase were 517%, 237%, 48.1%, 86.64% and 28.31% respectively. On the other hand, there was a marked decrease in serum albumin, by -36.41% and liver contents of reduced glutathione [GSH] by -79.5% after CCl4 treatment. The pineal hormone MLT and NAC were tested for their protective activity when each given alone and in combination together in cirrhotic rats. MLT, NAC and their combinations were significantly decreased levels of serum ALT [-25.5%, -15.7% and -29% respectively], serum AST [-22% for NAC alone and -16% for MLT+NAC], serum MDA [-33%, -30.5% and -43% respectively], liver MDA [-58%, -37% and -67.6% respectively] and serum NO [-21.5%, -17.5% and -26% respectively]. On opposite direction, MLT, NAC and their combinations were significantly increased liver GSH contents by 62%, 35% and 258% respectively. These results suggest that oxidative process occur at the site of cell integrity and are involved in the damage effect of CCl4 and indicate that free radicals may be a major component of liver cirrhosis. Likewise, MLT, NAC and their combination presumably due to their antioxidant and free radicals scavenging activity is highly protective against the biochemical changes associated with CCl4 treatment

Oxidative stress and interleukin-1 beta in serum and skin lesions of patients with generalized vitligo

The etiology of vitiligo is unknown. Increased oxidant stress may explain melanocyte dysfunction and destruction. Increases in pro-oxidants as well as decreases in anti-oxidant agents have been reported in patients with vitiligo. In this study we investigated the role of oxidative stress by determining the levels of the free radical nitric oxide [NO] and the antioxidant systems: superoxide dismutase [SOD], and L-ascorbic acid in addition to interleukin-1beta [IL-1beta] in both serum and tissue of lesional skin in patients with generalized vitiligo. Levels of NO and IL-1beta were significantly higher in the serum and tissue of lesional skin of patient with generalized vitiligo compared to the control group. While L-ascorbic acid and superoxide dismutase levels were significantly reduced in patients compared to controls. Extent of vitiligo showed a significant positive correlation with tissue levels of IL-1beta. Oxidative stress may play a role in the pathogenesis of generalized vitiligo with increased production of NO and decreased SOD activity and ascorbic acid levels. IL-1beta could have a role in the pathogenesis of vitiligo possibly through the induction of NO production

Lesional skin vascular endothelial growth factor levels correlate with the clinical severity in patients with cement allergic contact dermatitis

Allergic contact dermatitis to cement is a common occupational skin disease. It is a delayed-type hypersensitity reaction with Th1 type cytokine response. Interferon-gamma [IFN-gamma] is recognized as the main effector cytokine in contact hypersensitivity [CHS]. Vascular endothelial growth factor [VEGF] might be involved in persisting erythema and edema in eczematous skin. Human VEGF is a multifactorial cytokine that not only promotes angiogenesis but also enhances vascular permeability and participates in chronic inflammation. Thirty two building workers with chronic allergic contact dermatitis due to occupational exposure to cement and twenty healthy controls were included. The severity of eczema was assessed using the Eczema Area and Severity index [EASI]. VEGF and IFN-gamma in serum and skin lesions were measured in patients and healthy controls. Patients with cement allergic contact dermatitis showed significantly elevated levels of serum and lesional skin levels of VEGF compared to healthy controls [p=0.005 and p=0.001 respectively]. They also had significantly higher serum and tissue IFN-gamma levels compared to controls [p=0.007 and p=0.001 respectively. A significant positive correlation was demonstrated between skin tissue levels of VEGF and EASI score in patients with cement allergic contact dermatitis [r=0.86, p=0.001]. VEGF and IFN-gamma might play a role in the pathogenesis of cement allergic contact dermatitis. Lesional skin VEGF levels could be an indicator of the severity of eczema