title: Persistence of Staphylococcus aureus colonization on the skin of NC/Nga mice.
abstract: BACKGROUND
  Colonization of Staphylococcus aureus (S. aureus) on skin is one factor which can worsen atopic dermatitis (AD). The reduction of bacterial colonization in these lesions was reported to be effective for the treatment of subjects with AD. NC/Nga mice are recognized to be a model of AD.
  
  
  OBJECTIVE
  We examined the susceptibility of S. aureus colonization on the skin in NC/Nga mice, as compared with findings in BALB/c mice.
  
  
  METHODS
  The number of S. aureus on the skin was counted and serum corticosterone, serum interferon-gamma (IFN-gamma) and interleukin (IL)-12 levels were measured. The effects of dexamethasone on number of S. aureus on the skin and serum IFN-gamma and interleukin IL-12 levels were also examined.
  
  
  RESULTS
  The number of S. aureus increased in parallel with the severity of the dermatitis in these mice, and the remaining number of S. aureus on the skin after topical treatment of S. aureus suspension was higher than that in BALB/c mice. Serum IFN-gamma and IL-12 concentrations in NC/Nga mice were lower than in BALB/c mice, and the circadian variations of serum corticosterone concentrations in NC/Nga mice tended to reveal higher levels compared with the circadian variations in BALB/c mice. Continuous administration of dexamethasone inhibited the elimination of S. aureus from skin surfaces of BALB/c mice. Serum IFN-gamma and IL-12 concentrations in dexamethasone-treated BALB/c mice were lower than those in vehicle-treated BALB/c mice.
  
  
  CONCLUSIONS
  Our data support the notion that high levels of circadian variations of endogenous glucocorticoid lead to a lack of protection against bacteria and a persistence of S. aureus colonization on the skin in NC/Nga mice.
authors.affiliation: Pharmacology 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
authors.forename: Yuki
authors.initials: Y
authors.lastname: Hashimoto
authors.forename: Yoshie
authors.initials: Y
authors.lastname: Kaneda
authors.forename: Toshi
authors.initials: T
authors.lastname: Akashi
authors.forename: Iwao
authors.initials: I
authors.lastname: Arai
authors.forename: Shiro
authors.initials: S
authors.lastname: Nakaike
mesh_terms: D000818:Animals; D015169:Colony Count, Microbial; D003345:Corticosterone / Q000097:blood; D003876:Dermatitis, Atopic / Q000097:blood / Q000382:microbiology*; D003907:Dexamethasone / Q000494:pharmacology; D004195:Disease Models, Animal; D005938:Glucocorticoids / Q000494:pharmacology; D007371:Interferon-gamma / Q000096:biosynthesis / Q000097:blood; D018664:Interleukin-12 / Q000096:biosynthesis / Q000097:blood; D051379:Mice; D008815:Mice, Inbred Strains; D009994:Osmolar Concentration; D012720:Severity of Illness Index; D012867:Skin / Q000382:microbiology*; D013154:Spleen / Q000378:metabolism / Q000473:pathology; D013211:Staphylococcus aureus / Q000187:drug effects / Q000254:growth & development*
chemical_list: D005938:Glucocorticoids; D018664:Interleukin-12; D003907:Dexamethasone; D007371:Interferon-gamma; D003345:Corticosterone