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10:42
Generation and Culturing of Primary Human Keratinocytes from Adult Skin
Published on: December 22, 2017
Functional effects of interleukin 31 in human primary keratinocytes.
Sadaf Kasraie1, M Niebuhr, K Baumert
1Division of Immunodermatology and Allergy Research, Department of Dermatology and Allergy, Hannover Medical School, Hannover, Germany. kasraie.sadaf@mh-hannover.de
Allergy
|January 26, 2011
Summary
Interleukin-31 (IL-31) plays a role in human keratinocytes, with its receptor expression influenced by TLR-2 ligands. This interaction may be altered in atopic dermatitis (AD), impacting skin inflammation.
Area of Science:
- Dermatology
- Immunology
- Cell Biology
Background:
- Interleukin-31 (IL-31) is a cytokine primarily known for inducing pruritus in atopic dermatitis (AD).
- The inflammatory functions of IL-31 in human primary keratinocytes (HPKs) are not fully understood.
- IL-31 signals through a receptor comprising IL-31RA and OSMR, expressed on keratinocytes.
Purpose of the Study:
- To investigate the expression and regulation of the IL-31 receptor (IL-31RA and OSMR) in HPKs.
- To determine the functional effects of IL-31 stimulation on HPKs.
- To explore the link between IL-31 signaling and Toll-like receptor 2 (TLR-2) in HPKs, particularly in the context of AD.
Main Methods:
- HPKs were stimulated with TLR-2 ligands (Pam3Cys, lipoteichoic acid, peptidoglycan) or cytokines (IFN-γ, IL-4).
- IL-31 receptor expression and IL-31 signaling (STAT-3 phosphorylation) were analyzed at mRNA and protein levels.
- CCL2 secretion, TLR-2 expression, and STAT signaling were assessed using Western blot and immunohistochemistry.
Main Results:
- TLR-2 ligands and IFN-γ significantly upregulated IL-31RA and OSMR expression in HPKs.
- IL-31 stimulation activated STAT-3 phosphorylation, enhanced by pre-treatment with Pam3Cys or IFN-γ.
- IL-31 promoted CCL2 secretion following receptor upregulation, an effect impaired in keratinocytes from AD patients with reduced TLR-2 expression.
Conclusions:
- IL-31 has a functional role in HPKs, linking TLR-2 ligands to IL-31 signaling.
- This interaction may be dysregulated in AD, potentially contributing to cutaneous inflammation.
- Altered IL-31 function could be relevant in eczema, considering Staphylococcus aureus colonization and TLR-2 dysregulation in AD skin.
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