Oxidative Stress and Atopic Dermatitis

Bertino, Lucrezia; Guarneri, Fabrizio; Cannavò, Serafinella Patrizia; Casciaro, Marco; Pioggia, Giovanni; Gangemi, Sebastiano

doi:10.3390/antiox9030196

Cited by 93 publications

(72 citation statements)

References 68 publications

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“…Previous studies reported the involvement of ROS and lipid peroxidation in the pathogenesis of inflammatory skin diseases [ 19 , 36 , 37 , 38 , 39 ]. The relationship between oxidative stress and AD was recently revised [ 3 , 4 , 5 ]. Higher levels of MDA, a biomarker of lipid peroxidation, were demonstrated [ 10 ].…”

Section: Discussionmentioning

confidence: 99%

“…Although the pathogenesis of AD is not completely understood, genetic, environmental, and/or psychological triggers appear to be involved in and contribute to the infiltration of inflammatory cells, such as lymphocytes, macrophages, eosinophils, and mast cells [ 2 ]. The chronically inflamed skin of patients with atopic dermatitis plays a key role in the pathogenesis of this disease, with the overproduction of reactive oxygen species (ROS) [ 3 , 4 , 5 , 6 ]. The overproduction of ROS was observed in skin biopsies in AD patients compared to controls [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

“…The overproduction of ROS was observed in skin biopsies in AD patients compared to controls [ 6 ]. Studies in children and adults demonstrated higher levels of biomarkers of oxidative stress of lipids and nucleic acids in serum and urine [ 3 ]. Alterations of serum NO levels, malondialdehyde (MDA), and 8-hydroxydeoxyguanosine (8-OHdG) were described [ 5 , 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

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Oxidative Stress and Alterations of Paraoxonases in Atopic Dermatitis

Simonetti

Bacchetti

Ferretti³

et al. 2021

Antioxidants

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Background: previous studies reported the involvement of reactive oxygen species (ROS) and lipid peroxidation in the pathogenesis of inflammatory skin diseases. The aim of our study was to investigate the relationship between oxidative stress and inflammation in children affected by atopic dermatitis (AD), a chronic relapsing inflammatory skin disease. Methods: levels of lipid hydroperoxides, total antioxidant capacity, and activities of the enzymes myeloperoxidase (MPO), PON1, and PON2/3 were investigated in 56 atopic pediatric patients, and compared with 48 sex-/age-matched healthy controls. Results: significantly higher levels of lipid hydroperoxides and lower values of total antioxidant potential were observed in the serum of AD children compared to that of the controls. Significant lower PON1 activities, and a significant increase in levels of MPO were observed in serum of patients, with a higher serum MPO level/PON1 paraoxonase activity ratio in patients compared to that in the controls. Significantly lower lactonase activity of PON enzymes was observed in polymorphonuclear cells isolated from AD patients. Statistically negative correlation was established between the activity of intracellular PON2/3 activity and ROS levels. Conclusions: our data confirmed that AD is associated with higher oxidative damage and a decrease in antioxidant defense. Moreover, alterations of extracellular and intracellular PON activity can promote lipoprotein dysfunction in AD patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Oxidative Stress and Alterations of Paraoxonases in Atopic Dermatitis

Simonetti

Bacchetti

Ferretti³

et al. 2021

Antioxidants

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“…Haplopine inhibited the expressions of IL-4, IL-13, and COX-2, which were increased by oxidative stress in H 2 O 2 -treated Jurkat T cells. Dysregulation of antioxidant mechanisms contributes to oxidative stress, which is caused by an imbalance between ROS generation and activity of the antioxidant defense system [38][39][40], and reportedly, excessive oxidative stress is a major etiological factor of AD because it induces inflammatory genes such as IL-4, IL-13, and COX-2 [41][42][43][44]. Therefore, inhibition of oxidative stress may importantly alleviate AD by downregulating inflammatory mediator levels.…”

Section: Discussionmentioning

confidence: 99%

Haplopine Ameliorates 2,4-Dinitrochlorobenzene-Induced Atopic Dermatitis-Like Skin Lesions in Mice and TNF-α/IFN-γ-Induced Inflammation in Human Keratinocyte

Kim

Kim²,

Jegal

et al. 2021

Antioxidants

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This study aimed to investigate the anti-inflammatory, antioxidant, and anti-atopic dermatitis (AD) effects of haplopine, which is one of the active components in D. dasycarpus. Haplopine (12.5 and 25 mM) inhibited the mRNA expressions of inflammatory cytokines IL-6, TSLP, GM-CSF, and G-CSF and the protein expressions of IL-6 and GM-CSF in TNF-α/INF-γ-stimulated HaCaT cells. In H2O2-induced Jukat T cells, haplopine (25 and 50 mM) suppressed the productions of proinflammatory cytokines (IL-4, IL-13, and COX-2) and increased the mRNA and protein expressions of oxidative stress defense enzymes (SOD, CAT, and HO-1) in a concentration-dependent manner. In vivo, haplopine significantly attenuated the development of AD symptoms in 2,4-dinitrochlorobenzene (DNCB)-stimulated Balb/c mice, as evidenced by reduced clinical dermatitis scores, skin thickness measurements, mast cell infiltration, and serum IgE concentrations. These findings demonstrate that haplopine should be considered a novel anti-atopic agent with the potential to treat AD.

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“…As of now, we know that RAGE plays a role in a plethora of other physiological and pathological processes, including diabetes, osteoporosis and cardiovascular diseases. Over the course of time, many different factors, including oxidative stress, were studied to explain the pathophysiology of many skin diseases characterized by chronic inflammation and frequent relapses, such as atopic dermatitis [ 21 , 22 , 23 ], psoriasis [ 24 , 25 ], lichen planus [ 26 , 27 ], vitiligo [ 28 , 29 ], or discoid lupus erythematosus [ 30 ]. It is well known that the clinical expression of such diseases depends on a variety of factors, both inner and outer, but, as of yet, one of these factors, namely RAGE, seems to play an important role in a context of continuous inflammatory and autoimmune stimuli, thus prompting further studies in order to complete the picture we have of such diseases.…”

Section: Introductionmentioning

confidence: 99%

Involvement of RAGE and Oxidative Stress in Inflammatory and Infectious Skin Diseases

et al. 2021

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The surface receptor for advanced glycosylation end-products (RAGE) and its soluble (sRAGE) and endogenous secretory (EN-RAGE) forms belong to the superfamily of toll-like receptors and play important roles in inflammation and autoimmunity, directly or through binding with advanced glycosylation end-products (AGE) and advanced oxidation protein products (AOPP). We reviewed the literature on the role of RAGE in skin diseases. Research in this field is still rather limited (28 articles) but suggests the involvement of RAGE and RAGE-related pathways in chronic inflammatory diseases (lupus, psoriasis, atopic dermatitis, and lichen planus), infectious diseases (leprosy, Staphylococcus aureus-induced skin lesions), alterations of the repairing processes in diabetic skin, systemic sclerosis, and ulcers. These data prompt further research in this field, which not only will be useful to better understand the pathogenetic mechanisms of diseases, but is also likely to have intriguing clinical implications. Indeed, when their role in the complex and multifactorial inflammatory balance will be adequately defined, RAGE and related molecules could be used as markers of disease severity and/or response to treatment. Moreover, future promising therapeutic perspectives could be topical administration of some of these molecules (e.g., sRAGE) to modulate local inflammatory response and/or the development of anti-RAGE antibodies for systemic treatment.

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Oxidative Stress and Atopic Dermatitis

Cited by 93 publications

References 68 publications

Oxidative Stress and Alterations of Paraoxonases in Atopic Dermatitis

Oxidative Stress and Alterations of Paraoxonases in Atopic Dermatitis

Haplopine Ameliorates 2,4-Dinitrochlorobenzene-Induced Atopic Dermatitis-Like Skin Lesions in Mice and TNF-α/IFN-γ-Induced Inflammation in Human Keratinocyte

Involvement of RAGE and Oxidative Stress in Inflammatory and Infectious Skin Diseases

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