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Effects of chloromethylisothiazolinone/methylisothiazolinone (CMIT/MIT) on Th2/Th17-related immune modulation in an

Han-Na Go1, Seung-Hwa Lee1, Hyun-Ju Cho2

  • 1Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea.

Scientific Reports
|March 7, 2020
PubMed

Insights

Chloromethylisothiazolinone/methylisothiazolinone (CMIT/MIT) exposure worsens atopic dermatitis (AD) symptoms in mice. This occurs through the disruption of T-helper 2 (Th2) and T-helper 17 (Th17) immune responses, suggesting a link between CMIT/MIT and AD development.

Area of Science:

  • Immunology
  • Dermatology
  • Toxicology

Background:

  • Chloromethylisothiazolinone/methylisothiazolinone (CMIT/MIT) are preservatives linked to allergic contact dermatitis and occupational asthma.
  • Previous research has not investigated the impact of CMIT/MIT exposure on the development of atopic dermatitis (AD).
  • Understanding the role of environmental chemicals in AD pathogenesis is crucial for public health.

Purpose of the Study:

  • To investigate the effects of epicutaneous CMIT/MIT exposure on AD development in a mouse model.
  • To elucidate the underlying biological mechanisms contributing to CMIT/MIT-induced AD-like symptoms.

Main Methods:

  • BALB/C mice were subjected to CMIT/MIT epicutaneous exposure for three weeks.
  • Atopic dermatitis (AD) was induced using ovalbumin (OVA) epidermal sensitization.
  • Analysis included assessment of AD-like phenotypes, serum immunoglobulin E levels, inflammatory cell infiltration, and gene/protein expression of cytokines and immune cells in skin and lymph nodes.

Main Results:

  • CMIT/MIT exposure significantly exacerbated AD-like phenotypes, including increased transepidermal water loss, clinical scores, and inflammatory cell infiltration.
  • Exposure elevated mRNA expression of T helper (Th) 2 cytokines (TSLP, IL-6, IL-13) and Th2 chemokine (CCL17), along with an increased population of CD4+IL-4+ cells in the skin.
  • In OVA-challenged mice, CMIT/MIT exposure further augmented AD-like phenotypes and increased IL-4 and IL-17A mRNA expression and CD4+IL-4+- and IL-17A+-producing cells in skin-draining lymph nodes.

Conclusions:

  • Epicutaneous exposure to CMIT/MIT can induce and worsen AD-like symptoms in a mouse model.
  • CMIT/MIT exposure appears to dysregulate Th2 and Th17-related immune responses, contributing to AD pathogenesis.
  • These findings suggest a potential role for CMIT/MIT in the development or exacerbation of atopic dermatitis.

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