Differential modulation of stress-inflammation responses by plant polyphenols in cultured normal human keratinocytes and immortalized HaCaT cells

J Dermatol Sci. 2011 Aug;63(2):104-14. doi: 10.1016/j.jdermsci.2011.04.011. Epub 2011 May 8.

Abstract

Background: Environmental and endogenous stresses to skin are considered causative reasons for skin cancers, premature ageing, and chronic inflammation. Screening of substances with preventive and/or curative properties is currently based on mechanistic studies of their effects towards stress-induced responses in skin cell cultures.

Objective: We compared effects of plant polyphenols (PPs) on the constitutive, UVA-, LPS-, or TNF-alpha-induced inflammatory responses in cultured normal human epidermal keratinocytes (NHEK) and immortalized HaCaT cells.

Methods: Representatives of three classes of PPs, flavonoids, stilbenoids, and phenylpropanoids were studied. Their effects on mRNA were determined by qRT-PCR; protein expression was assayed by Western blot and bioplexed ELISA; phosphorylation of Akt1, ERK1/2, EGFR, and NFkappaB was quantified by intracellular ELISA or Western blot.

Results: PPs or their combination with UVA or LPS induced strong up-regulation of stress responses in HaCaT but not in NHEK. In addition, compared to NHEK, HaCaT responded to TNF-alpha with higher synthesis of MCP-1, IP-10 and IL-8, concomitant with stronger NFkappaB activation. PPs down-regulated the chemokine release from both cell types, although with distinct effects on NFkappaB, Akt1, ERK, and EGFR activation.

Conclusion: Results of pharmacological screenings obtained by using HaCaT should be cautiously considered while extending them to primary keratinocytes from human epidermis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • Cells, Cultured
  • Chemokine CCL2 / biosynthesis
  • Chemokine CXCL10 / biosynthesis
  • ErbB Receptors / metabolism
  • Flavonoids / pharmacology*
  • Humans
  • Inflammation / metabolism*
  • Interleukin-8 / biosynthesis
  • Keratinocytes / drug effects*
  • Keratinocytes / metabolism
  • Lipopolysaccharides / pharmacology
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 3 / metabolism
  • NF-kappa B / metabolism
  • Phenols / pharmacology*
  • Plant Extracts / chemistry
  • Plant Extracts / pharmacology
  • Polyphenols
  • Proto-Oncogene Proteins c-akt / metabolism
  • Stress, Physiological / drug effects*
  • Tumor Necrosis Factor-alpha / metabolism
  • Ultraviolet Rays
  • Up-Regulation

Substances

  • CCL2 protein, human
  • CXCL10 protein, human
  • Chemokine CCL2
  • Chemokine CXCL10
  • Flavonoids
  • Interleukin-8
  • Lipopolysaccharides
  • NF-kappa B
  • Phenols
  • Plant Extracts
  • Polyphenols
  • Tumor Necrosis Factor-alpha
  • EGFR protein, human
  • ErbB Receptors
  • AKT1 protein, human
  • Proto-Oncogene Proteins c-akt
  • MAPK1 protein, human
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3