The role of interleukin-1ß and interleukin-33 in atopic dermatitis

Introduction: Interleukin-1 super family is a group of cytokines that play a role in the regulation of immune and inflammatory responses. Interleukin-33 is a member of this family and is known to induce expression of the T helper2 cytokines that are important players in atopic dermatitis. Aim: To evaluate the expression of interleukins-1ß and 33 as T helper2 cytokines inducers in patients with atopic dermatitis. Materials andMethods: This study included 20 atopic patients and 20 apparently healthy individuals serving as controls. Skin biopsies from all participants will be examined for detection of interleukins-1ß and 33 by ELISA technique.Results: Both interleukins were statistically higher (P<0.001) in patients than in controls. A statistically significant (P=0.011) highest levels of interleukin-33 was detected in severe cases of atopics when compared to mild and moderate cases. A significant correlation (r=0.632, P=0.003) between both interleukins was detected in atopics.Conclusions: This is the first study to evaluate both interleukin-1ß and33 together in atopic patients. Both interleukins could play a role in the recruitment of lymphocytes during the inflammatory reaction in atopic dermatitis and could be targeted in the treatment of resistant cases

Increased tissue leptin hormone level and mast cell count in skin tags: A possible role of adipoimmune in the growth of benign skin growths

Background: Skin tags (ST) are common tumors. They mainly consist of loose fibrous tissue and occur on the neck and major flexures as small, soft, pedunculated protrusions. Decrease in endocrine, hormone level and other factors are thought to play a role in the evolution of ST. Leptin is an adipocyte-derived hormone that acts as a major regulatory hormone for food intake and energy homeostasis. Leptin deficiency or resistance can result in profound obesity and diabetes in humans. A role of mast cell in the pathogenesis of ST is well recognized. Aims: To investigate the role of leptin in the pathogenesis of ST and to clarify whether there is a correlation between mast cell count and leptin level in ST. Methods: Forty-five skin biopsies were taken from 15 patients with ST. From each patient, a biopsy of a large ST (length >4 mm), a small ST (length <2 mm) and a normal skin biopsy (as a control) were taken. The samples were processed for leptin level. Skin biopsies were stained with hematoxylin and eosin and toluidine blue-uranyl nitrate metachromatic method for mast cell count was used. Results: There was a significant increased level of leptin in the ST compared to the normal skin. It was highly significant in small ST than in big ST (P = 0.0001) and it was highly significant in small and big ST compared to controls, P = 0.0001 and P = 0.001, respectively. There was a significant increase in mast cell count in the ST, which did not correlate with the increased levels of leptin. Conclusion: This is the first report to demonstrate that tissue leptin may play a role in the pathogenesis of ST. The significant increase in the levels of leptin and mast cell count in ST may indicate a possible role of adipoimmune in the benign skin growths

THE POSSIBLE ROLE OF TRAUMA IN SKIN TAGS THROUGH THE RELEASE OF MAST CELL MEDIATORS

Background: Skin tags (ST) are common benign tumors of the skin but their etiopathogenesis is not well understood. STs arise in sites subjected to trauma. It was proved that mast cells are recruited to sites of skin trauma and increase their tumor necrosis factor-α (TNF-α) content. Aim: STs are linked to obesity and frictional sites, but this has not been studied at the molecular level. We hypothesized that mast cells, TNF-α and its family member, TNF-related apoptosis-inducing ligand (TRAIL) might play a role in the pathogenesis of STs as a response to trauma. Materials and Methods: A study was done on 15 patients with STs. Two STs and a snip of normal skin were obtained in each subject. We counted the mast cells after Toluidine blue staining. Enzyme-linked immunosorbant assay was used to measure TNF-α level while reverse transcriptase polymerase chain reaction was used to evaluate the level of TRAIL mRNA expression. Results: Mast cell count in all STs was significantly higher than that in control (P=0.0355). There was a highly significant increase in the level of TNF-α in all STs as compared to its level in controls (P<0.0001). Expression of TRAIL mRNA was significantly higher in STs as compared to its expression in controls (P<0.0001). Conclusion: Our study suggests that mast cells, TNF-α and TRAIL may play a role in the pathogenesis of STs

Do prolactin and its receptor play a role in alopecia areata?

Context: Studying the link between prolactin and autoimmunity has gained much ground over the past years. Its role played in alopecia areata (AA) is not clear yet, as previous reports yielded controversial results. Aims: This study aimed to measure the serum level of prolactin and to detect the expression of its receptor in AA, in an attempt to highlight its possible role in the pathogenesis of this disease. Subjects and Methods: A case-control study of 30 AA patients and 20 controls from outpatient clinic were undertaken. Every patient was subjected to history taking and clinical examination to determine the severity of alopecia tool (SALT) score. Blood samples were taken from patients and controls to determine the serum prolactin level. Scalp biopsies were obtained from the lesional skin of patients and normal skin of controls for assessment of the prolactin receptor. Statistical Analysis: Depending upon the type of data, t-test, analysis of variance test, Chi-square, receiver operator characteristic curve were undertaken. Results: On comparing the serum prolactin level between patients and controls, no significant difference was found, while the mean tissue level of prolactin receptor was significantly higher in patients than in controls. In patients, a significant positive correlation was found between the prolactin receptor and the SALT score. Conclusions: Prolactin plays a role in AA, and this role is probably through the prolactin receptors rather than the serum prolactin level