NOD2 signalling in hidradenitis suppurativa

Area of Science:

• Immunodermatology
• Molecular Biology
• Genetics

Background:

• Hidradenitis suppurativa (HS) involves immune dysregulation, with altered cytokine, chemokine, and antimicrobial peptide (AMP) expression.
• The role of nucleotide-binding oligomerization domain-containing (NOD)2 signaling in HS pathogenesis is not well understood.

Purpose of the Study:

• To investigate the expression of NOD2 and associated factors in HS skin lesions and keratinocytes.
• To explore the potential role of NOD2 signaling in HS development and immune response.

Main Methods:

• Real-time PCR was used to quantify mRNA expression of NOD2, RIP2, CARL, SKALP/elafin, hBD2, LL37, psoriasin, and RNAse7.
• Analysis was performed on lesional and nonlesional skin from 19 HS patients and on cultured keratinocytes (unstimulated, MDP-stimulated, or Pam2-stimulated).

Main Results:

• Elevated mRNA expression of NOD2, hBD2, RNAse7, psoriasin, and SKALP/elafin was observed in lesional HS skin compared to nonlesional skin.
• Significant correlations were found between NOD2 mRNA and hBD2, psoriasin, and SKALP/elafin expression in HS skin.
• NOD2 signaling components showed altered expression patterns in HS keratinocytes compared to normal keratinocytes, with some factors significantly increased in HS cells.

Conclusions:

• This study provides the first evidence of activated NOD2 signaling in HS.
• NOD2 signaling may contribute to HS pathogenesis by inducing AMPs and activating pathways like nuclear factor-κB signaling.