Primary administration of Lactobacillus johnsonii NCC533 in weaning period suppresses the elevation of proinflammatory cytokines and CD86 gene expressions in skin lesions in NC/Nga mice.
The administration of probiotic lactic acid bacteria (LAB) has been studied for its potential to prevent atopic dermatitis (AD). The objective of this study was to assess the inhibitory mechanism of a skin lesion by LAB using an experimental model that we previously demonstrated in NC/Nga mice. Lactobacillus johnsonii NCC533 (La1) was administered orally to the La1 group from 20 to 22 days after birth, while phosphate-buffered saline was given to the control group. After the induction of skin lesions in 6-week-old mice, the expression of genes supposedly involved in AD was evaluated. Gene expression of the proinflammatory cytokines [interleukin-8 (IL-8), IL-12 and IL-23] was significantly enhanced in the lesional skin of the control group by the induction of the lesion, whereas gene expression of those in the La1 group was not elevated. Interestingly, expression of the costimulatory molecule CD86 showed a pattern similar to the expression of the cytokines in the lesional skin. Moreover, the La1 group showed a significantly lower gene expression of CD86 in Peyer's patches and mesenteric lymph nodes than the control group. The suppression of proinflammatory cytokines and CD86 by primary administration of La1 may significantly contribute to the inhibitory effect on the skin lesion.
Inoue
Ryo
R
Laboratory of Animal Science, Kyoto Prefectural University, Shimogamo Kyoto, Japan.
Otsuka
Mai
M
Nishio
Ayako
A
Ushida
Kazunari
K
D000284:Administration, Oral; D000818:Animals; D015703:Antigens, CD / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D000943:Antigens, Differentiation / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D018122:B7-1 Antigen / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D051940:B7-2 Antigen / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D018106:CD28 Antigens / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D060908:CTLA-4 Antigen; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D003876:Dermatitis, Atopic / Q000235:genetics / Q000276:immunology* / Q000473:pathology / Q000517:prevention & control; D005260:Female; D015870:Gene Expression; D018928:Immunity, Mucosal; D007378:Interleukins / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D007778:Lactobacillus / Q000276:immunology*; D008221:Lymphoid Tissue / Q000276:immunology / Q000473:pathology; D051379:Mice; D008925:Mites / Q000276:immunology; D011247:Pregnancy; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D014886:Weaning
D015703:Antigens, CD; D000943:Antigens, Differentiation; D018122:B7-1 Antigen; D051940:B7-2 Antigen; D018106:CD28 Antigens; D060908:CTLA-4 Antigen; C497965:Cd86 protein, mouse; C556707:Ctla4 protein, mouse; D016207:Cytokines; D007378:Interleukins