THE CAUSAL RELATIONSHIP BETWEEN OXIDATIVE STRESS AND TYPE 2 INFLAMMATION IN ATOPIC DERMATITIS: A NARRATIVE REVIEW
Atopic dermatitis (AD) is a chronic, recurrent inflammatory disease with a multifactorial etiology involving genetic, environmental, and immunological factors. Among the immunopathological mechanisms, the type 2 inflammatory response stands out, mediated primarily by the cytokines IL-4, IL-5, and IL-13, which contribute to skin barrier dysfunction. In particular, interleukins IL-4 and IL-13 inhibit barrier proteins, inducing oxidative stress, which can be defined as a result of the imbalance between the production of reactive oxygen species and the body’s antioxidant mechanisms, intensifying Th2 polarization and the production of inflammatory mediators. This cycle perpetuates the inflammatory process, amplifying symptoms such as eczema and pruritus. To better elucidate the immunopathological mechanisms linking oxidative stress and type 2 inflammation in AD, as well as to demonstrate the pathophysiological mechanisms of type 2 inflammation in atopic dermatitis, address the effects of oxidative stress associated with the development of type 2 inflammation, and identify the process of oxidative stress modulation in the development of atopic dermatitis, a narrative review with a qualitative and descriptive approach was conducted, based on articles found in the following databases: BVS, PubMed, ScienceDirect, and Academia.edu. The data suggest that epidermal barrier dysfunction and reduced filaggrin expression are central to the pathogenesis of AD, favoring the penetration of environmental irritants and inducing a type 2 response. This process is exacerbated by oxidative stress, which intensifies Th2 polarization and perpetuates the inflammatory cycle, worsening eczema and pruritus in AD by further polarizing the type 2 response.
THE CAUSAL RELATIONSHIP BETWEEN OXIDATIVE STRESS AND TYPE 2 INFLAMMATION IN ATOPIC DERMATITIS: A NARRATIVE REVIEW
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DOI: https://doi.org/10.22533/at.ed.5157282602048
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Palavras-chave: Type 2 inflammation; Oxidative stress; Atopic dermatitis.
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Keywords: Type 2 inflammation; Oxidative stress; Atopic dermatitis.
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Abstract:
Atopic dermatitis (AD) is a chronic, recurrent inflammatory disease with a multifactorial etiology involving genetic, environmental, and immunological factors. Among the immunopathological mechanisms, the type 2 inflammatory response stands out, mediated primarily by the cytokines IL-4, IL-5, and IL-13, which contribute to skin barrier dysfunction. In particular, interleukins IL-4 and IL-13 inhibit barrier proteins, inducing oxidative stress, which can be defined as a result of the imbalance between the production of reactive oxygen species and the body’s antioxidant mechanisms, intensifying Th2 polarization and the production of inflammatory mediators. This cycle perpetuates the inflammatory process, amplifying symptoms such as eczema and pruritus. To better elucidate the immunopathological mechanisms linking oxidative stress and type 2 inflammation in AD, as well as to demonstrate the pathophysiological mechanisms of type 2 inflammation in atopic dermatitis, address the effects of oxidative stress associated with the development of type 2 inflammation, and identify the process of oxidative stress modulation in the development of atopic dermatitis, a narrative review with a qualitative and descriptive approach was conducted, based on articles found in the following databases: BVS, PubMed, ScienceDirect, and Academia.edu. The data suggest that epidermal barrier dysfunction and reduced filaggrin expression are central to the pathogenesis of AD, favoring the penetration of environmental irritants and inducing a type 2 response. This process is exacerbated by oxidative stress, which intensifies Th2 polarization and perpetuates the inflammatory cycle, worsening eczema and pruritus in AD by further polarizing the type 2 response.
- Sabrina Lucietti Dick
- LAURA BERLITZ
- MARIA EDUARDA RIBAS BISSANI
- PHELIPE DOS SANTOS SOUZA
- CLAUDIA DOS SANTOS DUTRA BERNHARDT
