scholarly journals High Calcium, ATP, and Poly(I:C) Augment the Immune Response to β-Glucan in Normal Human Epidermal Keratinocytes

2011 ◽  
Vol 131 (11) ◽  
pp. 2255-2262 ◽  
Author(s):  
Carren Sy Hau ◽  
Yayoi Tada ◽  
Sayaka Shibata ◽  
Hideya Uratsuji ◽  
Yoshihide Asano ◽  
...  
Keyword(s):  
Immune Response ◽  
Poly I:C ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Normal Human Epidermal Keratinocytes ◽  
High Calcium ◽  
Normal Human

TLR3 agonists Poly(I:C) enhances melanosome uptake by normal human epidermal keratinocytes

2017 ◽  
Vol 86 (2) ◽  
pp. e84
Author(s):  
Saaya Koike ◽  
Kenshi Yamasaki ◽  
Takeshi Yamauchi ◽  
Kenichiro Tsutiyama ◽  
Setsuya Aiba
Keyword(s):  
Poly I:C ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Normal Human Epidermal Keratinocytes ◽  
Normal Human

scholarly journals C3a and Its Receptor C3aR Are Detectable in Normal Human Epidermal Keratinocytes and Are Differentially Regulated via TLR3 and LL37

2021 ◽  
pp. 1-15
Author(s):  
Susanne Mommert ◽  
Lisa Doenni ◽  
Phillip Szudybill ◽  
Christoph Zoeller ◽  
Frerk Hinnerk Beyer ◽  
...  
Keyword(s):  
Biologically Active ◽  
Poly I:C ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Complement Components ◽  
Expression Levels ◽  
Normal Human Epidermal Keratinocytes ◽  
Intracellular Expression ◽  
Normal Human ◽  
Anaphylatoxin C3a

To study the molecular interplay between TLRs and complement representing ancient danger-sensing mechanisms, we examined the regulation of the C3a/anaphylatoxin C3a receptor (C3aR) axis in normal human epidermal keratinocytes (NHEKs) by treatment with different TLR ligands. Protein staining followed by flow cytometry revealed highly constitutive intracellular expression levels of the C3aR in NHEKs. Stimulation with Poly I:C up-regulated C3aR mRNA and intra- and extracellular expression in NHEKs which showed functional relevance by up-regulating CXCL10 and down-regulating C3 expression in response to C3a. mRNA and protein levels of C3 and protease cathepsin L (CTSL) that can cleave C3 were up-regulated by the TLR3 ligand Poly I:C. Enhanced intracellular expression levels of the biologically active C3 fragment (C3a), in response to TLR3 stimulation were also detectable in NHEKs. Cathelicidin antimicrobial peptide LL-37 potentiated Poly I:C-induced C3aR, C3, and CTSL up-regulation. In conclusion, we point to a role of TLR3 to promote up-regulation of C3aR, C3, and CTSL expression levels and generation of C3a. Our data provide evidence that local generation and activation of complement components as described for T cells or myeloid cells represent a scenario which may take place in a similar way in NHEKs.

scholarly journals Psoriasis-Associated Inflammatory Conditions Induce IL-23 mRNA Expression in Normal Human Epidermal Keratinocytes

2022 ◽  
Vol 23 (1) ◽  
pp. 540
Author(s):  
Evelyn Kelemen ◽  
Éva Ádám ◽  
Stella Márta Sági ◽  
Anikó Göblös ◽  
Lajos Kemény ◽  
...  
Keyword(s):  
Nucleic Acid ◽  
Nucleic Acids ◽  
Mrna Expression ◽  
Signaling Pathways ◽  
Poly I:C ◽  
Psoriatic Skin ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Normal Human Epidermal Keratinocytes ◽  
Normal Human

Psoriasis is a multifactorial, chronic inflammatory skin disease, the development of which is affected by both genetic and environmental factors. Cytosolic nucleic acid fragments, recognized as pathogen- and danger-associated molecular patterns, are highly abundant in psoriatic skin. It is known that psoriatic skin exhibits increased levels of IL-23 compared to healthy skin. However, the relationship between free nucleic acid levels and IL-23 expression has not been clarified yet. To examine a molecular mechanism by which nucleic acids potentially modulate IL-23 levels, an in vitro system was developed to investigate the IL-23 mRNA expression of normal human epidermal keratinocytes under psoriasis-like circumstances. This system was established using synthetic nucleic acid analogues (poly(dA:dT) and poly(I:C)). Signaling pathways, receptor involvement and the effect of PRINS, a long non-coding RNA previously identified and characterized by our research group, were analyzed to better understand the regulation of IL-23 in keratinocytes. Our results indicate that free nucleic acids regulate epithelial IL-23 mRNA expression through the TLR3 receptor and specific signaling pathways, thereby, contributing to the development of an inflammatory milieu favorable for the appearance of psoriatic symptoms. A moderate negative correlation was confirmed between the nucleic-acid-induced IL-23 mRNA level and the rate of its decrease upon PRINS overexpression.

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