In vivo quantitative analysis of advanced glycation end products in atopic dermatitis-Possible culprit for the

Ji Yeon Hong1, Min Jeong Kim2, Jun Ki Hong2

  • 1Department of Dermatology, Seoul National University Hospital, Seoul, Korea.

Insights

Advanced glycation end products (AGEs) accumulate in the skin of atopic dermatitis (AD) patients, fueling inflammation. Reduced levels of AGEs

Area of Science:

  • Dermatology
  • Immunology
  • Biochemistry

Background:

  • Advanced glycation end products (AGEs) trigger inflammatory responses via the receptor for AGEs (RAGE).
  • Soluble RAGE (sRAGE) and endogenous secretory RAGE (esRAGE) act as decoys, mitigating AGE-induced inflammation and offering cytoprotection.

Purpose of the Study:

  • To investigate the expression of AGEs and their receptors (RAGE, sRAGE, esRAGE) in the serum and skin of patients with atopic dermatitis (AD).
  • To correlate AGE and receptor levels with AD severity.

Main Methods:

  • A case-control study involving 29 adult AD patients and 12 healthy controls.
  • Quantification of AGE, sRAGE, and esRAGE levels in serum and corneocytes using Enzyme-Linked Immunosorbent Assay (ELISA).
  • Comparison of levels between AD patients and controls, and correlation with AD severity.

Main Results:

  • Corneocyte AGE levels were significantly elevated in AD patients compared to controls (P = .002).
  • Higher corneocyte AGE levels were associated with more severe AD.
  • Serum AGE levels showed no significant difference between groups.
  • Serum sRAGE levels were markedly decreased in AD patients (P = .007), with a similar trend observed for serum esRAGE.

Conclusions:

  • Dermal accumulation of AGEs may contribute to skin inflammation in atopic dermatitis.
  • Reduced levels of sRAGE and esRAGE in AD patients suggest a diminished capacity to neutralize AGEs.
  • Further research is needed to evaluate the systemic risks associated with reduced AGE neutralizers in AD.

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