Tumor necrosis factor α-308 G/A and interleukin 1 β-511 C/T gene polymorphisms in patients with scarring acne

J Cosmet Dermatol. 2019 Feb;18(1):395-400. doi: 10.1111/jocd.12558. Epub 2018 Apr 19.

Abstract

Background: Acne is a chronic inflammatory skin disorder which may heal with scarring. Tumor necrosis factor alpha (TNF α) and interleukin 1 β (IL-1β) are considered as the main responsible proinflammatory mediators of acne pathogenesis. Oversecretion of these cytokines was found to be associated with TNF α-308 G>A and IL-1β-511 C<T polymorphisms.

Aim: To evaluate the association of TNF α-308 and IL-1β-511 gene polymorphisms with acne and postacne scarring susceptibility and acne severity.

Methods: Study subjects included 90 patients with acne vulgaris (31 males, 59 females; mean age: 19.6 ± 3.7 years) and 30 healthy controls (11 males, 19 females; mean age: 19.2 ± 5.1 years). Patients were sub-grouped on the basis of acne severity into mild, moderate, and severe acne groups and on the presence postacne scarring into scarring acne and nonscarring acne groups. Peripheral venous blood samples were obtained for performing real-time PCR analysis for detecting TNF α-308 and IL-1β-511 genotypic variants.

Results: Among patients, 21.7% (n = 26) had mild, 22.5% (n = 27) had moderate, 30.8% (n = 37) had severe, and 30% (n = 36) had scarring acne. Genotypic variants of TNF α-308 and IL-1β-511 did not statistically differ between acne patients and controls (P values: .245 and .466). When compared in terms of acne severity and the presence of postacne scarring, no statistical significance was observed regarding frequencies of genotypic variants related to the both TNF α-308 and IL-1β polymorphisms (P > .05).

Conclusion: TNF α-308 and IL-1β polymorphic variants are not associated with acne and postacne scarring susceptibility and acne severity.

Keywords: IL-1β; TNF α; acne; polymorphism; scarring.

MeSH terms

  • Acne Vulgaris / complications
  • Acne Vulgaris / genetics*
  • Adolescent
  • Case-Control Studies
  • Cicatrix / etiology
  • Female
  • Genotype
  • Humans
  • Interleukin-1beta / genetics*
  • Male
  • Polymorphism, Genetic
  • Severity of Illness Index
  • Tumor Necrosis Factor-alpha / genetics*
  • Young Adult

Substances

  • IL1B protein, human
  • Interleukin-1beta
  • Tumor Necrosis Factor-alpha