Persistence of Staphylococcus aureus colonization on the skin of NC/Nga mice

Yuki Hashimoto1, Yoshie Kaneda, Toshi Akashi

  • 1Pharmacology Laboratory, Medical Research Laboratories, Taisho Pharmaceutical Co., Ltd., 1-403, Yoshino-cho, Kita-ku, Saitama-city, Saitama 331-9530, Japan. yuki.hashimoto@po.rd.taisho.co.jp

Abstract

Insights

NC/Nga mice show increased Staphylococcus aureus (S. aureus) colonization, linked to atopic dermatitis severity. High corticosterone levels in these mice impair bacterial clearance, unlike in BALB/c mice.

Area of Science:

  • Immunology
  • Microbiology
  • Dermatology

Background:

  • Staphylococcus aureus (S. aureus) colonization exacerbates atopic dermatitis (AD).
  • Reducing bacterial load in AD lesions can improve treatment outcomes.
  • NC/Nga mice serve as a relevant animal model for studying AD.

Purpose of the Study:

  • To compare S. aureus skin colonization susceptibility between NC/Nga and BALB/c mice.
  • To investigate the role of immune markers and corticosterone in S. aureus persistence.
  • To evaluate the impact of dexamethasone on bacterial load and immune responses.

Main Methods:

  • Quantified S. aureus skin colonization in NC/Nga and BALB/c mice.
  • Measured serum corticosterone, interferon-gamma (IFN-γ), and interleukin-12 (IL-12) levels.
  • Assessed the effects of dexamethasone on bacterial counts and immune markers.

Main Results:

  • S. aureus colonization correlated with dermatitis severity in NC/Nga mice.
  • NC/Nga mice exhibited higher S. aureus persistence and lower serum IFN-γ and IL-12 levels compared to BALB/c mice.
  • Elevated corticosterone circadian variations were observed in NC/Nga mice; dexamethasone impaired S. aureus clearance in BALB/c mice.

Conclusions:

  • High circadian variations in endogenous glucocorticoids contribute to impaired bacterial defense and persistent S. aureus colonization in NC/Nga mice.
  • These findings highlight a potential mechanism linking stress hormones, immune dysfunction, and bacterial susceptibility in AD models.