Interference of Skin Scratching Attenuates Accumulation of Neutrophils in Murine Allergic Contact Dermatitis Model
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ORIGINAL ARTICLE
Interference of Skin Scratching Attenuates Accumulation of Neutrophils in Murine Allergic Contact Dermatitis Model Hiroyasu Sakai,1,5 Taku Ishida,1 Ken Sato,2 Kazutaka Mandokoro,3 Saori Yabe,1 Fumiaki Sato,2 Yoshihiko Chiba,4 Risako Kon,1 Nobutomo Ikarashi,1 and Junzo Kamei1
Abstract— We recently reported that swelling resulting from 2,4,6-trinitrochlorobenzene
(TNCB) challenge might be associated with recruitment of neutrophils. However, it is not known whether neutrophil recruitment is affected by scratching at inflamed sites or not. Therefore, the effects of an Elizabethan collar on the TNCB-induced upregulation of ELRpositive chemokines (CXCL1, CXCL2, and CXCL5) and neutrophil recruitment were investigated. Mice were sensitized by the application of TNCB on abdominal skin. Then, the mice were challenged three times with TNCB to auricle of the ear. To prevent scratching at inflamed sites, an Elizabethan collar was placed on the mice from just before the first challenge until the end of the experiment. The effects of the Elizabethan collar on the TNCB-induced upregulation of CXCLs chemokines and recruitment of neutrophil were investigated. The increase of ear swelling by TNCB challenge was inhibited by the Elizabethan collar. TNCB-challenge-induced upregulation of TNF-α, IL-1β, IL-6, ELR+ chemokines, MPO, and ELA2 was also attenuated by the Elizabethan collar. The gene expression of CXCL1, CXCL2, and CXCL5 human homolog IL-8 was enhanced by TNFα and IL-1β in human dermal fibroblasts and epidermal keratinocytes. We here suggest that scratching the site of inflammation leads to neutrophil accumulation mediated by TNF-α and IL-1β/ELR+ chemokines in TNCB-challenge-induced contact dermatitis in mice. KEY WORDS: allergic contact dermatitis; itch sensation; skin scratching; chemokine; neutrophil.
INTRODUCTION 1
Department of Biomolecular Pharmacology, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan 2 Department of Analytical Pathophysiology, School of Pharmacy, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan 3 Department of Pharmacology, School of Pharmacy, Hoshi University, 24-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan 4 Department of Physiology and Molecular Sciences, School of Pharmacy, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan 5 To whom correspondence should be addressed at Department of Biomolecular Pharmacology, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan. E-mail: [email protected]
Allergic contact dermatitis (ACD) develops after someone encounters an allergen or hapten, which is a small molecule. ACD potentially leads to itching, swelling, redness, and rash. Common causes of ACD include perfume, eye shadow, nail polish, lipstick, some sunscreens, and dyes in clothing. CD is, thus, a frequent occupational skin disease and one of the major environmental health problems in developed countries [4, 12]. CD is classified as a
0360-3997/19/0000-0001/0 # 2019 Springer Science+Business Media, LLC, part
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