Interference of Skin Scratching Attenuates Accumulation of Neutrophils in Murine Allergic Contact Dermatitis Model

Inflammation. 2019 Dec;42(6):2226-2235. doi: 10.1007/s10753-019-01086-y.

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 ELR-positive 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 TNF-α 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.

Keywords: allergic contact dermatitis; chemokine; itch sensation; neutrophil; skin scratching.

MeSH terms

  • Animals
  • Dermatitis, Allergic Contact / pathology*
  • Disease Models, Animal
  • Gene Expression Regulation / drug effects
  • Humans
  • Interleukin-1beta / metabolism
  • Interleukin-1beta / pharmacology
  • Mice
  • Neutrophil Infiltration*
  • Picryl Chloride
  • Pruritus
  • Skin / injuries*
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Interleukin-1beta
  • Tumor Necrosis Factor-alpha
  • Picryl Chloride