title: Oral treatment with probiotic Lactobacillus johnsonii NCC533 (La1) for a specific part of the weaning period prevents the development of atopic dermatitis induced after maturation in model mice, NC/Nga.
abstract: BACKGROUND
  The inhibitory effect of probiotic bacteria on atopic dermatitis has been shown in human infants, but the mechanism is still unclear.
  
  
  OBJECTIVE
  This study aimed to show the effects of the administration of a probiotic during the weaning period in mouse models on production of the intestinal secretory IgA (sIgA) and on the development of atopic dermatitis (AD) in later life.
  
  
  METHODS
  The effects of the administration of Lactobacillus johnsonii NCC533 (La1) during weaning were evaluated using a mouse model (Balb/c). The weaning period of mice was divided into three phases according to the evolution of faecal IgA. La1 was administered in each phase and the evolution of the faecal IgA was estimated. In the next experiment, the effect of the administration of La1 in phase 2 on host immunity after maturation was further assessed by using the model NC/Nga mouse for human AD.
  
  
  RESULTS
  Administration of La1 in each phase showed a distinct effect on the production of sIgA. But sIgA production was only positively stimulated when La1 was administrated in phase 2. The development of AD induced by mite antigen from 6 weeks old was significantly prevented by the primary administration of La1 in phase 2. AD-like lesions were significantly milder than those of the control mice, and histological observations showed an almost normal appearance of the epidermis and upper dermis of the mice treated with La1.
  
  
  CONCLUSIONS
  This study suggested that the primary administration of La1 in a specific part of the weaning period is effective in preventing or inhibiting the development of AD after maturation by modulating or accelerating the gut immune response.
authors.affiliation: Laboratory of Animal Science, Kyoto Prefectural University, Shimogamo, Kyoto, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Inoue
authors.forename: A
authors.initials: A
authors.lastname: Nishio
authors.forename: Y
authors.initials: Y
authors.lastname: Fukushima
authors.forename: K
authors.initials: K
authors.lastname: Ushida
mesh_terms: D000818:Animals; D039741:Antigens, Dermatophagoides / Q000276:immunology; D003876:Dermatitis, Atopic / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D004334:Drug Administration Schedule; D005243:Feces / Q000737:chemistry; D005260:Female; D007071:Immunoglobulin A, Secretory / Q000096:biosynthesis; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007422:Intestines / Q000276:immunology; D007778:Lactobacillus; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D019936:Probiotics / Q000008:administration & dosage / Q000627:therapeutic use*; D014886:Weaning
chemical_list: D039741:Antigens, Dermatophagoides; D007071:Immunoglobulin A, Secretory; D007074:Immunoglobulin G; D007073:Immunoglobulin E