title: Orally supplemented Lactobacillus acidophilus strain L-92 inhibits passive and active cutaneous anaphylaxis as well as 2,4-dinitroflurobenzene and mite fecal antigen induced atopic dermatitis-like skin lesions in mice.
abstract: Oral supplementation of lactic acid bacteria is a potential approach to the prevention and manipulation of allergic diseases such as atopic dermatitis. Our previous report showed that heat-killed Lactobacillus acidophilus strain L-92 (L-92) possessed anti-allergic properties, although its physiological function in atopic dermatitis has largely remained undefined. To evaluate the anti-allergic efficacy of L-92, we used four experimental animal models with the major features of atopic dermatitis and compared the results to those of clinically active drugs. ICR mice were passively sensitized by anti-dinitrophenyl mouse monoclonal IgE for passive cutaneous anaphylaxis (PCA), and BALB/c mice were actively sensitized by ovalbumin for active cutaneous anaphylaxis (ACA). Allergic reaction was induced by repeated exposure to 2,4-dinitroflurobenzene (DNFB) and mite (Dermatophagoides farinae) fecal allergen, in BALB/c and NC/Nga mice, respectively. Orally administrated L-92 significantly inhibited the vascular permeability increase in both PCA and ACA, and the elevation of ovalbumin-specific IgE titer in ACA. Moreover, repeated applications of DNFB and mite fecal antigen onto the BALB/c and NC/Nga mouse ear, respectively, caused clinical symptoms similar to atopic dermatitis such as ear swelling, scratching behavior and elevation of total serum IgE levels that were also moderately suppressed by L-92. In addition, L-92 treated mice exhibited lower levels of mast cells, eosinophil infiltration and Th1/Th2 cytokine expression. Our results, therefore, suggest that oral administration of L-92 might be useful for alleviating allergic symptoms.
authors.affiliation: Laboratory of Bioresponses and Regulation, United Graduate School of Drug Discovery and Medical Information Science, Gifu University, 1-1 Yanagido, Gifu 501-1193, Japan.
authors.forename: Mohammad Monir
authors.initials: MM
authors.lastname: Shah
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Miyamoto
authors.forename: Yoshihito
authors.initials: Y
authors.lastname: Yamada
authors.forename: Hirotaka
authors.initials: H
authors.lastname: Yamashita
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Tanaka
authors.forename: Takayuki
authors.initials: T
authors.lastname: Ezaki
authors.forename: Hiroichi
authors.initials: H
authors.lastname: Nagai
authors.forename: Naoki
authors.initials: N
authors.lastname: Inagaki
mesh_terms: D000284:Administration, Oral; D000707:Anaphylaxis / Q000517:prevention & control*; D000818:Animals; D039741:Antigens, Dermatophagoides / Q000633:toxicity*; D016207:Cytokines / Q000096:biosynthesis; D003876:Dermatitis, Atopic / Q000517:prevention & control*; D004139:Dinitrofluorobenzene / Q000633:toxicity*; D005260:Female; D007073:Immunoglobulin E / Q000096:biosynthesis; D007779:Lactobacillus acidophilus; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008813:Mice, Inbred ICR; D010323:Passive Cutaneous Anaphylaxis; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D039741:Antigens, Dermatophagoides; D016207:Cytokines; D007073:Immunoglobulin E; D004139:Dinitrofluorobenzene