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ELR + chemokine‐mediated neutrophil recruitment is involved in 2,4,6‐trinitrochlorobenzene‐induced contact hypersensitivity
Author(s) -
Sakai Hiroyasu,
Yabe Saori,
Sato Ken,
Kai Yuki,
Sato Fumiaki,
Yumoto Tetsuro,
Inoue Yuka,
Narita Minoru,
Matsumoto Kenjiro,
Kato Shinichi,
Chiba Yoshihiko
Publication year - 2018
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12839
Subject(s) - chemokine , immunology , cxcl1 , myeloperoxidase , dermis , infiltration (hvac) , medicine , chemistry , inflammation , pathology , physics , thermodynamics
Contact dermatitis is a form of delayed‐type hypersensitivity characterized by localized thickening, papules, redness and vesicles of the skin. A model of contact dermatitis involving repeated challenge of a hapten is adapted to assess dermatitis as characterized by skin thickening. Recently, it was reported that neutrophils have crucial roles in contact hypersensitivity. We thus examined the involvement of CXC chemokines bearing the glutamic acid–leucine–arginine ( ELR ) motif (“ ELR + chemokines”) and neutrophils in the ear swelling induced by 2,4,6‐trinitrochlorobenzene ( TNCB ) challenges in the present study. Mice were sensitized by application of TNCB on their abdominal skin. They were then challenged thrice with TNCB to the ear. The CXCR 2 antagonist SB 225002 (9 mg/kg, i.p.) was administered before each TNCB challenge. Gene expressions and protein levels of the ELR + chemokines CXCL 1, 2 and 5 was increased markedly in mouse ear after the final TNCB challenge. In addition, we indicated that gene expression of CXCL 1 was enhanced in the epidermis and dermis upon TNCB challenge. Expression of the CXCL 2 gene was enhanced in the epidermis, and that of the CXCL 5 gene was enhanced in the dermis. The swelling induced by TNCB challenges was significantly attenuated by SB 225002. Furthermore, the increases in myeloperoxidase activity, and expression of myeloperoxidase and neutrophil elastase induced by TNCB challenge in mouse ear were inhibited by SB 225002. These data suggest that ear swelling resulting from TNCB challenges might be concerned by upregulated ELR + chemokine‐induced neutrophil recruitment.