Activation of Eosinophils Interacting with Dermal Fibroblasts by Pruritogenic Cytokine IL-31 and Alarmin IL-33: Implications in Atopic Dermatitis : Dr. Wong

Activation of Eosinophils Interacting with Dermal Fibroblasts by Pruritogenic Cytokine IL-31 and Alarmin IL-33: Implications in Atopic Dermatitis.

Author Interview: Dr. CK Wong

Professor Department of Chemical Pathology
The Chinese University of Hong Kong
Prince of Wales Hospital
Shatin, NT  Hong Kong

What are the main findings of the study?

This experimental study evaluated the novel immunopathological role of pruritogenic IL-31 in conjunction with alarmin IL-33 upon the interaction of human eosinophils and dermal fibroblasts at local inflammatory sites in atopic dermatitis (AD). Our results demonstrated a stimulatory effect induced by co-culture of eosinophils and fibroblasts on cytokine and AD-related chemokines release. The above stimulatory effects could be significantly enhanced by the AD-related IL-31 and IL-33, probably via the intercellular adhesion molecule-1 cell surface expression and differential intracellular signaling mechanisms in co-culture.

Were any of the findings unexpected?

We observed the synergistic induction of AD-related chemokines in co-culture of eosinophils and dermal fibroblasts upon stimulation by IL-31 and IL-33 together.

What should clinicians and patients take away from this study?

As IL-31 and IL-33 play crucial role in AD, the circulating level of IL-31 and IL-33 may serve as specific disease markers for monitoring AD severity and therapeutic efficacy.

For AD patients, the induction of pruritogenic cytokine IL-31 may result in scratching-mediated tissue damage for the release of alarmin IL-33, these two cytokines subsequently together activate the infiltrating eosinophils interacting with dermal fibroblasts for allergic inflammation in affected skin.

What recommendations do you have for future research as a result of your study?

Future study for the IL-31 and IL-33 activating effects on skin-resident eosinophils and dermal fibroblasts obtained from AD patients is needed.

Nevertheless, our findings and established co-culture platform will facilitate the future development of selective inhibitors for cytokines and intracellular signaling molecules for the treatment of AD and inflammatory diseases.  Further animal model studies are also on-going.

Reference:

Activation of Eosinophils Interacting with Dermal Fibroblasts by Pruritogenic Cytokine IL-31 and Alarmin IL-33: Implications in Atopic Dermatitis.

Wong C-K, Leung KM-L, Qiu H-N, Chow JY-S, Choi AOK, et al.
PLoS ONE 7(1): e29815. doi:10.1371/journal.pone.0029815   (2012)

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