Indian Journal of Dermatology Venereology & Leprology最新文献

Objective To investigate the protective effects of an angiotensin-converting enzyme inhibitor after inducing oxidative stress on keloid fibroblasts. Methods Primary keloid fibroblasts were isolated and cultured by enzyme digestion combined with the tissue adhesion method in vitro, and the third to fifth generations of cells were selected for the experiment. For 24 hours, keloid fibroblasts were treated with different concentrations of hydrogen peroxide. Different concentrations of angiotensin-converting enzyme inhibitor were added to the keloid fibroblast culture medium, and then the cells were treated with hydrogen peroxide for 24 hours. Results With the increase of hydrogen peroxide concentration, the growth of keloid fibroblasts was inhibited and the levels of malondialdehyde, superoxide dismutase, and reactive oxygen species increased gradually, accompanied by an increase in the expression of nicotinamide adenine dinucleotide phosphate oxidase and collagen I mRNA. The expression of nicotinamide adenine dinucleotide phosphate oxidase-mRNA in keloid fibroblasts and the formation of reactive oxygen species in keloid fibroblasts were induced by different concentrations of angiotensin II, and the most significant effect was at 10-5 mmol/mL. The effects of diphenyleneiodonium chloride (NOX inhibitor), N-acetylcysteine (reactive oxygen species inhibitor) and nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) RNA treatment on angiotensin II-induced nicotinamide adenine dinucleotide phosphate oxidase and collagen I increased significantly. Hydrogen peroxide and angiotensin II alone or combined can induce NADPH oxidase and reactive oxygen species expression in keloid fibroblasts. When the angiotensin-converting enzyme inhibitor was added, the expression of NADPH oxidase and reactive oxygen species in keloid induced by hydrogen peroxide and angiotensin II could be inhibited. Conclusion Oxidative stress can lead to increased expression of reactive oxygen species, NADPH oxidase and collagen I in keloid fibroblasts, suggesting oxidative stress mediates the migration of human keloid fibroblasts and extracellular matrix synthesis.

Background Considering the cross-regulation of Th1 and Th2 responses, we hypothesised that atopic diseases (Th2) inhibit the protective Th1 immune response to Mycobacterium leprae and exacerbates leprosy. Objective In this study, we aimed to evaluate the association between leprosy and atopic diseases. Methods To evaluate the association of atopic diseases with leprosy, we conducted a case-control study that included leprosy patients (n = 333) and their household contacts (n = 93). The questionnaire from the International Study of Asthma and Allergies in Childhood, which is validated in several countries for epidemiological diagnosis of atopic diseases, was applied to determine the occurrence of atopic diseases, allergic rhinitis, asthma, and atopic dermatitis among leprosy patients and the household contacts. Results Considering clinical and epidemiological data, among the leprosy group 51.6% (n = 172) were determined to have at least one atopic disease, while atopy was observed less frequently at 40.86% among household contacts (n = 38). When two or more atopic diseases were assessed, the frequency was significantly higher among the leprosy patients than in the household contacts (21.9% vs. 11.8%; P-value = 0.03). Likewise, the frequency of asthma was significantly higher among leprosy patients (21%) than in the household contacts (10.8%; P-value = 0.02). Thus, our analyses revealed an association of atopic diseases with leprosy, with a significant linear increase in the occurrence of leprosy with an increase in the number of atopic diseases (P-value = 0.01). Limitation Due to the difficulties in recruiting household contacts that have prolonged contact with patients, but are not genetically related to the patient, the household contacts group is smaller than the leprosy patient group. Conclusion The data reveal an association between atopic diseases and leprosy outcomes. This knowledge could improve the treatment of leprosy patients with co-incident atopic diseases.