Lack of interleukin-33 and its receptor does not prevent calcipotriol-induced atopic dermatitis-like inflammation in mice.

Abstract:

:Current studies addressing the influence of interleukin-33 or its receptor (IL-33R/ST2) on development of atopic dermatitis-like inflammation in mice have reported conflicting results. We compared the response in single- and double-deficient IL-33-/-/ST2-/- C57BL/6J BomTac mice in the well-established calcipotriol-induced model of atopic dermatitis. All genotypes (groups of up to 14 mice) developed atopic dermatitis-like inflammation yet we observed no biologically relevant difference between groups in gross anatomy or ear thickness. Moreover, histological examination of skin revealed no differences in mononuclear leukocyte and granulocyte infiltration nor Th2 cytokine levels (IL-4 and IL-13). Finally, skin CD45+ cells and CD3+ cells were found at similar densities across all groups. Our findings indicate that lack of interleukin-33 and its receptor ST2 does not prevent the development of AD-like skin inflammation.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Pietka W,Sundnes O,Hammarström C,Zucknick M,Khnykin D,Haraldsen G

doi

10.1038/s41598-020-63410-z

subject

Has Abstract

pub_date

2020-04-15 00:00:00

pages

6451

issue

1

issn

2045-2322

pii

10.1038/s41598-020-63410-z

journal_volume

10

pub_type

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