Toll-like receptor signalling induces the expression of serum amyloid A in epidermal keratinocytes and dermal fibroblasts

S. Morizane, A. Kajita, K. Mizuno, T. Takiguchi, K. Iwatsuki

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Background: Toll-like receptors (TLRs) play critical roles in innate immune response by sensing pathogen- or damage-associated molecular patterns. Epidermal keratinocytes and dermal fibroblasts also produce proinflammatory cytokines and chemokines under stimulation with TLR ligands. Serum amyloid A (SAA) is an essential factor in the pathogenesis of secondary amyloidosis, and also has immunomodulatory functions. SAA are produced mainly by hepatocytes but also by a variety of cells, including immune cells, endothelial cells, synoviocytes, and epidermal keratinocytes. However, SAA expression in human dermal fibroblasts has not been shown to date. Aim: To investigate the effect of TLR ligands on SAA expression in epidermal keratinocytes and dermal fibroblasts. Methods: We investigated whether TLR ligands induce the expression of SAA in normal human epidermal keratinocytes (NHEKs) and normal human dermal fibroblasts (NHDFs) by real-time quantitative PCR and ELISA. The effect of SAA on its own expression in NHDFs was also studied. Results: SAA expression was induced via nuclear factor-κB by TLR1/2, 3, 5 and 2/6 ligands in NHEKs. In NHDFs, TLR1/2 and TLR2/6 ligands increased SAA expression. SAA further induced its own expression via TLR1/2 and NF-κB in NHDFs, as previously reported for NHEKs. Conclusions: Our results provide new evidence that the skin's innate immune response contributes to the production of SAA, which might lead to an increased risk of systemic complications such as secondary amyloidosis of recessive dystrophic epidermolysis bullosa.

Original languageEnglish
JournalClinical and Experimental Dermatology
DOIs
Publication statusAccepted/In press - Jan 1 2018

Fingerprint

Serum Amyloid A Protein
Toll-Like Receptors
Keratinocytes
Fibroblasts
Skin
Ligands
Amyloidosis
Innate Immunity
Epidermolysis Bullosa Dystrophica
Chemokines
Real-Time Polymerase Chain Reaction
Hepatocytes
Endothelial Cells
Enzyme-Linked Immunosorbent Assay
Cytokines

ASJC Scopus subject areas

  • Dermatology

Cite this

@article{1ba446ed376b40afaaaabd260757795d,
title = "Toll-like receptor signalling induces the expression of serum amyloid A in epidermal keratinocytes and dermal fibroblasts",
abstract = "Background: Toll-like receptors (TLRs) play critical roles in innate immune response by sensing pathogen- or damage-associated molecular patterns. Epidermal keratinocytes and dermal fibroblasts also produce proinflammatory cytokines and chemokines under stimulation with TLR ligands. Serum amyloid A (SAA) is an essential factor in the pathogenesis of secondary amyloidosis, and also has immunomodulatory functions. SAA are produced mainly by hepatocytes but also by a variety of cells, including immune cells, endothelial cells, synoviocytes, and epidermal keratinocytes. However, SAA expression in human dermal fibroblasts has not been shown to date. Aim: To investigate the effect of TLR ligands on SAA expression in epidermal keratinocytes and dermal fibroblasts. Methods: We investigated whether TLR ligands induce the expression of SAA in normal human epidermal keratinocytes (NHEKs) and normal human dermal fibroblasts (NHDFs) by real-time quantitative PCR and ELISA. The effect of SAA on its own expression in NHDFs was also studied. Results: SAA expression was induced via nuclear factor-κB by TLR1/2, 3, 5 and 2/6 ligands in NHEKs. In NHDFs, TLR1/2 and TLR2/6 ligands increased SAA expression. SAA further induced its own expression via TLR1/2 and NF-κB in NHDFs, as previously reported for NHEKs. Conclusions: Our results provide new evidence that the skin's innate immune response contributes to the production of SAA, which might lead to an increased risk of systemic complications such as secondary amyloidosis of recessive dystrophic epidermolysis bullosa.",
author = "S. Morizane and A. Kajita and K. Mizuno and T. Takiguchi and K. Iwatsuki",
year = "2018",
month = "1",
day = "1",
doi = "10.1111/ced.13604",
language = "English",
journal = "Clinical and Experimental Dermatology",
issn = "0307-6938",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Toll-like receptor signalling induces the expression of serum amyloid A in epidermal keratinocytes and dermal fibroblasts

AU - Morizane, S.

AU - Kajita, A.

AU - Mizuno, K.

AU - Takiguchi, T.

AU - Iwatsuki, K.

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Background: Toll-like receptors (TLRs) play critical roles in innate immune response by sensing pathogen- or damage-associated molecular patterns. Epidermal keratinocytes and dermal fibroblasts also produce proinflammatory cytokines and chemokines under stimulation with TLR ligands. Serum amyloid A (SAA) is an essential factor in the pathogenesis of secondary amyloidosis, and also has immunomodulatory functions. SAA are produced mainly by hepatocytes but also by a variety of cells, including immune cells, endothelial cells, synoviocytes, and epidermal keratinocytes. However, SAA expression in human dermal fibroblasts has not been shown to date. Aim: To investigate the effect of TLR ligands on SAA expression in epidermal keratinocytes and dermal fibroblasts. Methods: We investigated whether TLR ligands induce the expression of SAA in normal human epidermal keratinocytes (NHEKs) and normal human dermal fibroblasts (NHDFs) by real-time quantitative PCR and ELISA. The effect of SAA on its own expression in NHDFs was also studied. Results: SAA expression was induced via nuclear factor-κB by TLR1/2, 3, 5 and 2/6 ligands in NHEKs. In NHDFs, TLR1/2 and TLR2/6 ligands increased SAA expression. SAA further induced its own expression via TLR1/2 and NF-κB in NHDFs, as previously reported for NHEKs. Conclusions: Our results provide new evidence that the skin's innate immune response contributes to the production of SAA, which might lead to an increased risk of systemic complications such as secondary amyloidosis of recessive dystrophic epidermolysis bullosa.

AB - Background: Toll-like receptors (TLRs) play critical roles in innate immune response by sensing pathogen- or damage-associated molecular patterns. Epidermal keratinocytes and dermal fibroblasts also produce proinflammatory cytokines and chemokines under stimulation with TLR ligands. Serum amyloid A (SAA) is an essential factor in the pathogenesis of secondary amyloidosis, and also has immunomodulatory functions. SAA are produced mainly by hepatocytes but also by a variety of cells, including immune cells, endothelial cells, synoviocytes, and epidermal keratinocytes. However, SAA expression in human dermal fibroblasts has not been shown to date. Aim: To investigate the effect of TLR ligands on SAA expression in epidermal keratinocytes and dermal fibroblasts. Methods: We investigated whether TLR ligands induce the expression of SAA in normal human epidermal keratinocytes (NHEKs) and normal human dermal fibroblasts (NHDFs) by real-time quantitative PCR and ELISA. The effect of SAA on its own expression in NHDFs was also studied. Results: SAA expression was induced via nuclear factor-κB by TLR1/2, 3, 5 and 2/6 ligands in NHEKs. In NHDFs, TLR1/2 and TLR2/6 ligands increased SAA expression. SAA further induced its own expression via TLR1/2 and NF-κB in NHDFs, as previously reported for NHEKs. Conclusions: Our results provide new evidence that the skin's innate immune response contributes to the production of SAA, which might lead to an increased risk of systemic complications such as secondary amyloidosis of recessive dystrophic epidermolysis bullosa.

UR - http://www.scopus.com/inward/record.url?scp=85047466229&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85047466229&partnerID=8YFLogxK

U2 - 10.1111/ced.13604

DO - 10.1111/ced.13604

M3 - Article

C2 - 29770468

AN - SCOPUS:85047466229

JO - Clinical and Experimental Dermatology

JF - Clinical and Experimental Dermatology

SN - 0307-6938

ER -