start-ver=1.4
cd-journal=joma
no-vol=44
cd-vols=
no-issue=1
article-no=
start-page=40
end-page=46
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=20180516
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Toll‐like receptor signalling induces the expression of serum amyloid A in epidermal keratinocytes and dermal fibroblasts
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=BACKGROUND:</br>
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.</br>
AIM:</br>
To investigate the effect of TLR ligands on SAA expression in epidermal keratinocytes and dermal fibroblasts.</br>
METHODS:</br>
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.</br>
RESULTS:</br>
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.</br>
CONCLUSIONS:</br>
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.
en-copyright=
kn-copyright=

en-aut-name=MorizaneS.
en-aut-sei=Morizane
en-aut-mei=S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KajitaA.
en-aut-sei=Kajita
en-aut-mei=A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MizunoK.
en-aut-sei=Mizuno
en-aut-mei=K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=Takiguchi T.
en-aut-sei=Takiguchi 
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IwatsukiK.
en-aut-sei=Iwatsuki
en-aut-mei=K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
END