Regulation of human eosinophil-dermal fibroblast interaction by fundamental innate immunity inhibitor IL-37 in atopic dermatitis
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The interaction between eosinophils (EOS) and dermal fibroblasts is a central cellular
pathway for the induction of allergic inflammation via distinct intracellular signaling
mechanisms, which is the crucial part of the immunopathological mechanism in atopic
dermatitis (AD).
Human eosinophils and dermal fibroblast (HDF) co-culture system was used to investigate
inflammatory cytokines/chemokines secretion upon AD-related IL-31/IL-33 stimulation,
while the autophagy signaling proteins were analysed by Western blot. CRISPR/Cas9 human
IL37 knock-in mice were bred for MC903-induced AD model in vivo. Ear swelling and EOS
infiltration were assessed by H&E staining and immunohistochemistry. The snatching times
were recorded to evaluate itching severity. Serum cytokines and chemokines and spleen
regulatory T (Treg) cell were determined by flow cytometry.
IL-37 significantly inhibited IL-6 and CXCL8 production in co-culture system and autophagy
related protein expression, showing IL-37 might reduce the inflammation through autophagy
signal pathway (all p < 0.05). However, no autophagy process was detected in either EOS or
HDF alone culture, suggesting interaction between EOS and HDF is essential for the
autophagy mechanism in the resolution of allergic inflammation. Ear swelling was reduced
10.79% and 15.32% of IL-37 Tg group at Day 15 and Day 17 comparing with control wild
type mice, respectively. The EOS number in ear of IL-37 Tg group was much lower than that
of control group. Importantly, IL-37 significantly ameliorated the itching state, which is an
intolerable clinical feature of AD. Multiplex assay showed the serum AD-related cytokines
and chemokines level of IL-37 Tg group was much lower, while Treg cells in spleen of IL-37
Tg group was much higher comparing with control group, suggesting IL-37 might reduce
allergic inflammation by increasing immunosuppressive Treg cells in vivo.
IL-37 could significantly ameliorate MC903-induced AD symptom by inhibiting eosinophils
infiltration as well as eosinophils-induced allergic inflammation, suggesting IL-37 could be a
promising anti-inflammatory agent for AD.
All Author(s) ListTH HOU, J ZHU, KL HON, CK WONG
Name of Conference24th Annual Scientific Meeting, Hong Kong Society of Flow Cytometry
Start Date of Conference09/03/2019
End Date of Conference09/03/2019
Place of ConferenceHong Kong
Country/Region of ConferenceHong Kong
LanguagesEnglish-United Kingdom

Last updated on 2020-04-05 at 15:17