Upregulation of IL-36 cytokines in folliculitis and eosinophilic pustular folliculitis

Seisho Sato, Takahito Chiba, Takeshi Nakahara, Masutaka Furue

Research output: Contribution to journalArticle

Abstract

Background: Members of the interleukin (IL)-36 family, IL-36α, IL-36β and IL-36γ, are potent chemoattractive cytokines for neutrophils and eosinophils. IL-36 receptor antagonist (IL-36Ra) inhibits IL-36α, IL-36β and IL-36γ activity. However, the immunohistological expression of IL-36α, IL-36β, IL-36γ and IL-36Ra has never been addressed in normal follicles, folliculitis or eosinophilic pustular folliculitis (EPF). Methods: We performed immunohistochemical staining for IL-36α, IL-36β, IL-36γ and IL-36Ra using 10 cases of EPF, nine of non-specific folliculitis, 10 normal skin samples and 10 samples of normal follicles adjacent to a sebaceous naevus as a control. Two dermatologists, who were blind to the patient records, evaluated all of the slides. Results: The immunoreactive IL-36α was hardly detected in the follicular epithelium and epidermis in the normal skin, folliculitis or EPF. The expression of IL-36β, IL-36γ and IL-36Ra was augmented in both folliculitis and EPF compared with that in normal follicles. Negative correlations were detected between IL-36β and IL-36Ra and between IL-36γ and IL-36Ra in normal follicles; however, these were absent in folliculitis. In contrast to normal follicles and folliculitis, a significant positive correlation between IL-36β/γ and IL-36Ra was shown in EPF. Conclusions: The overexpression of IL-36β, IL-36γ and IL-36Ra is an integral part of the inflammatory response of folliculitis and EPF. The coordinated expression of IL-36γ and IL-36Ra may be related to the pathomechanism of EPF.

Original languageEnglish
JournalAustralasian Journal of Dermatology
DOIs
Publication statusAccepted/In press - Jan 1 2019

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Folliculitis
Interleukins
Up-Regulation
Cytokines
Eosinophilic pustular folliculitis

All Science Journal Classification (ASJC) codes

  • Dermatology

Cite this

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title = "Upregulation of IL-36 cytokines in folliculitis and eosinophilic pustular folliculitis",
abstract = "Background: Members of the interleukin (IL)-36 family, IL-36α, IL-36β and IL-36γ, are potent chemoattractive cytokines for neutrophils and eosinophils. IL-36 receptor antagonist (IL-36Ra) inhibits IL-36α, IL-36β and IL-36γ activity. However, the immunohistological expression of IL-36α, IL-36β, IL-36γ and IL-36Ra has never been addressed in normal follicles, folliculitis or eosinophilic pustular folliculitis (EPF). Methods: We performed immunohistochemical staining for IL-36α, IL-36β, IL-36γ and IL-36Ra using 10 cases of EPF, nine of non-specific folliculitis, 10 normal skin samples and 10 samples of normal follicles adjacent to a sebaceous naevus as a control. Two dermatologists, who were blind to the patient records, evaluated all of the slides. Results: The immunoreactive IL-36α was hardly detected in the follicular epithelium and epidermis in the normal skin, folliculitis or EPF. The expression of IL-36β, IL-36γ and IL-36Ra was augmented in both folliculitis and EPF compared with that in normal follicles. Negative correlations were detected between IL-36β and IL-36Ra and between IL-36γ and IL-36Ra in normal follicles; however, these were absent in folliculitis. In contrast to normal follicles and folliculitis, a significant positive correlation between IL-36β/γ and IL-36Ra was shown in EPF. Conclusions: The overexpression of IL-36β, IL-36γ and IL-36Ra is an integral part of the inflammatory response of folliculitis and EPF. The coordinated expression of IL-36γ and IL-36Ra may be related to the pathomechanism of EPF.",
author = "Seisho Sato and Takahito Chiba and Takeshi Nakahara and Masutaka Furue",
year = "2019",
month = "1",
day = "1",
doi = "10.1111/ajd.13143",
language = "English",
journal = "Australasian Journal of Dermatology",
issn = "0004-8380",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Upregulation of IL-36 cytokines in folliculitis and eosinophilic pustular folliculitis

AU - Sato, Seisho

AU - Chiba, Takahito

AU - Nakahara, Takeshi

AU - Furue, Masutaka

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Background: Members of the interleukin (IL)-36 family, IL-36α, IL-36β and IL-36γ, are potent chemoattractive cytokines for neutrophils and eosinophils. IL-36 receptor antagonist (IL-36Ra) inhibits IL-36α, IL-36β and IL-36γ activity. However, the immunohistological expression of IL-36α, IL-36β, IL-36γ and IL-36Ra has never been addressed in normal follicles, folliculitis or eosinophilic pustular folliculitis (EPF). Methods: We performed immunohistochemical staining for IL-36α, IL-36β, IL-36γ and IL-36Ra using 10 cases of EPF, nine of non-specific folliculitis, 10 normal skin samples and 10 samples of normal follicles adjacent to a sebaceous naevus as a control. Two dermatologists, who were blind to the patient records, evaluated all of the slides. Results: The immunoreactive IL-36α was hardly detected in the follicular epithelium and epidermis in the normal skin, folliculitis or EPF. The expression of IL-36β, IL-36γ and IL-36Ra was augmented in both folliculitis and EPF compared with that in normal follicles. Negative correlations were detected between IL-36β and IL-36Ra and between IL-36γ and IL-36Ra in normal follicles; however, these were absent in folliculitis. In contrast to normal follicles and folliculitis, a significant positive correlation between IL-36β/γ and IL-36Ra was shown in EPF. Conclusions: The overexpression of IL-36β, IL-36γ and IL-36Ra is an integral part of the inflammatory response of folliculitis and EPF. The coordinated expression of IL-36γ and IL-36Ra may be related to the pathomechanism of EPF.

AB - Background: Members of the interleukin (IL)-36 family, IL-36α, IL-36β and IL-36γ, are potent chemoattractive cytokines for neutrophils and eosinophils. IL-36 receptor antagonist (IL-36Ra) inhibits IL-36α, IL-36β and IL-36γ activity. However, the immunohistological expression of IL-36α, IL-36β, IL-36γ and IL-36Ra has never been addressed in normal follicles, folliculitis or eosinophilic pustular folliculitis (EPF). Methods: We performed immunohistochemical staining for IL-36α, IL-36β, IL-36γ and IL-36Ra using 10 cases of EPF, nine of non-specific folliculitis, 10 normal skin samples and 10 samples of normal follicles adjacent to a sebaceous naevus as a control. Two dermatologists, who were blind to the patient records, evaluated all of the slides. Results: The immunoreactive IL-36α was hardly detected in the follicular epithelium and epidermis in the normal skin, folliculitis or EPF. The expression of IL-36β, IL-36γ and IL-36Ra was augmented in both folliculitis and EPF compared with that in normal follicles. Negative correlations were detected between IL-36β and IL-36Ra and between IL-36γ and IL-36Ra in normal follicles; however, these were absent in folliculitis. In contrast to normal follicles and folliculitis, a significant positive correlation between IL-36β/γ and IL-36Ra was shown in EPF. Conclusions: The overexpression of IL-36β, IL-36γ and IL-36Ra is an integral part of the inflammatory response of folliculitis and EPF. The coordinated expression of IL-36γ and IL-36Ra may be related to the pathomechanism of EPF.

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U2 - 10.1111/ajd.13143

DO - 10.1111/ajd.13143

M3 - Article

AN - SCOPUS:85070809063

JO - Australasian Journal of Dermatology

JF - Australasian Journal of Dermatology

SN - 0004-8380

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