Anti-inflammatory effects of differential molecular weight Hyaluronic acids on UVB-induced calprotectin-mediated keratinocyte inflammation.
Calprotectin
Damage-associated molecular
Hyaluronic acid
Inflammation
Molecular weight
Patterns(DAMPs)
UVB
Journal
Journal of dermatological science
ISSN: 1873-569X
Titre abrégé: J Dermatol Sci
Pays: Netherlands
ID NLM: 9011485
Informations de publication
Date de publication:
Jul 2022
Jul 2022
Historique:
received:
13
10
2021
revised:
09
05
2022
accepted:
03
06
2022
pubmed:
19
6
2022
medline:
31
8
2022
entrez:
18
6
2022
Statut:
ppublish
Résumé
The biological functions of Hyaluronic acid are related to its molecular weight and binding to its receptor, Toll-like receptor4 (TLR4) or CD44. Recent studies have shown that low-molecular-weight Hyaluronic acid (LMW-HA) exhibits proinflammatory effects, while high-molecular-weight Hyaluronic acid (HMW-HA) functions as an anti-inflammatory factor. UVB-induced epidermal inflammation is mainly mediated by endogenous molecules, such as damage-associated molecular patterns (DAMPs), that cause severe skin damage by activating TLR signaling pathways. Since both LMW- and HMW-HA have inhibitory functions on TLR-mediated macrophage inflammation, HA is assumed to suppress UVB-induced DAMP-mediated inflammation in the skin. In this study, both Ultra- low-molecular-weight Hyaluronic acid (uLMW-HA) and HMW-HA were found to inhibit UVB-induced keratinocyte inflammation. HaCaT cells were treated with medium containing Hyaluronic acid at the appropriate concentration after 15 mJ/cm By competitively binding to TLR4, uLMW-HA downregulated Calprotectin-induced TRAF6 expression, which might be the direct process by which uLMW-HA decreased UVB-induced IL-6 secretion. Reduced CD44 variant (CD44v) expression in keratinocytes attenuated the inhibitory effect of both uLMW-HA and HMW-HA on UVB-induced inflammation, which indicated the involvement of CD44v in HA-regulated anti-inflammatory activity. Overall, this research indicates that Hyaluronic acid is more than a moisturizer; it is also a biologically effective material that can prevent the excessive skin inflammation caused in daily life, especially in the late stages after sunburn.
Sections du résumé
BACKGROUND
BACKGROUND
The biological functions of Hyaluronic acid are related to its molecular weight and binding to its receptor, Toll-like receptor4 (TLR4) or CD44. Recent studies have shown that low-molecular-weight Hyaluronic acid (LMW-HA) exhibits proinflammatory effects, while high-molecular-weight Hyaluronic acid (HMW-HA) functions as an anti-inflammatory factor. UVB-induced epidermal inflammation is mainly mediated by endogenous molecules, such as damage-associated molecular patterns (DAMPs), that cause severe skin damage by activating TLR signaling pathways.
OBJECTIVE
OBJECTIVE
Since both LMW- and HMW-HA have inhibitory functions on TLR-mediated macrophage inflammation, HA is assumed to suppress UVB-induced DAMP-mediated inflammation in the skin. In this study, both Ultra- low-molecular-weight Hyaluronic acid (uLMW-HA) and HMW-HA were found to inhibit UVB-induced keratinocyte inflammation.
METHODS
METHODS
HaCaT cells were treated with medium containing Hyaluronic acid at the appropriate concentration after 15 mJ/cm
RESULTS
RESULTS
By competitively binding to TLR4, uLMW-HA downregulated Calprotectin-induced TRAF6 expression, which might be the direct process by which uLMW-HA decreased UVB-induced IL-6 secretion. Reduced CD44 variant (CD44v) expression in keratinocytes attenuated the inhibitory effect of both uLMW-HA and HMW-HA on UVB-induced inflammation, which indicated the involvement of CD44v in HA-regulated anti-inflammatory activity.
CONCLUSION
CONCLUSIONS
Overall, this research indicates that Hyaluronic acid is more than a moisturizer; it is also a biologically effective material that can prevent the excessive skin inflammation caused in daily life, especially in the late stages after sunburn.
Identifiants
pubmed: 35717315
pii: S0923-1811(22)00158-X
doi: 10.1016/j.jdermsci.2022.06.001
pii:
doi:
Substances chimiques
Anti-Inflammatory Agents
0
Leukocyte L1 Antigen Complex
0
Toll-Like Receptor 4
0
Hyaluronic Acid
9004-61-9
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
24-31Informations de copyright
Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The corresponding author had full access to all the data in the study and had final responsibility for the decision to submit for publication. Jun Muto M.D., Ph.D. declares that he serves as a scientific advisor for RHOTO pharmaceutical CO. Ltd. The other authors declare they are employee of RHOTO pharmaceutical CO. Ltd.