Dietary supplementation with lactic acid bacteria attenuates the development of atopic-dermatitis-like skin lesions in NC/Nga mice in a strain-dependent manner.
BACKGROUND
Dietary supplementation with lactic acid bacteria (LAB) is a potential approach to the prevention and manipulation of allergic diseases such as atopic dermatitis (AD). However, the influence of different bacterial strains and their immunomodulating capacities is still largely unknown.


METHODS
AD-like skin lesions were induced by sensitization to and repeated challenges with picrylchloride in the Th2-skewed NC/Nga mouse strain. The effects of LAB supplementation were assessed over time by monitoring clinical scores and plasma IgE levels. In some cases, mast cell infiltration, cutaneous hypersensitivity responses and cytokine mRNA expression in auricles were also examined. Additionally, cytokine production in vitro and cytokine mRNA accumulation in major lymphoid tissues were measured, comparing Lactobacillus paracasei KW3110 with L. rhamnosus GG (LGG).


RESULTS
Supplementation with KW3110 significantly reduced the development of AD-like skin lesions, accompanied by less mast cell infiltration and lower plasma IgE levels. KW3110 also suppressed immediate hypersensitivity reactions and IL-4 mRNA expression in the auricles. These preventive effects sustained when supplementation was terminated; moreover, inhibitory effects were also observed even when supplementation was initiated after the onset of symptoms. In accordance with its effects on IL-12 and IL-4 production in vitro, KW3110 prevented the emergence of clinical symptoms more effectively than LGG in vivo.


CONCLUSIONS
Supplementation with KW3110 significantly attenuated the onset and exacerbation of AD-like symptoms in NC/Nga mice. The effects were more prominent than those obtained with LGG, suggesting the importance of differences between LAB strains and their immunomodulating capacity.
Wakabayashi
Hideyuki
H
Central Laboratories for Frontier Technology, Kirin Brewery Co., Ltd., Yokohama, Japan. hwakabayashi@kirin.co.jp
Nariai
Chie
C
Takemura
Fumiyo
F
Nakao
Wakako
W
Fujiwara
Daisuke
D
D000818:Animals; D003876:Dermatitis, Atopic / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D004431:Ear, External; D006968:Hypersensitivity, Delayed / Q000276:immunology / Q000517:prevention & control; D006969:Hypersensitivity, Immediate / Q000276:immunology / Q000517:prevention & control; D007073:Immunoglobulin E / Q000097:blood; D007371:Interferon-gamma / Q000096:biosynthesis / Q000235:genetics; D018664:Interleukin-12 / Q000096:biosynthesis / Q000235:genetics; D015847:Interleukin-4 / Q000096:biosynthesis / Q000235:genetics; D007778:Lactobacillus / Q000502:physiology*; D052201:Lacticaseibacillus rhamnosus / Q000502:physiology*; D008198:Lymph Nodes / Q000378:metabolism / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000473:pathology; D051379:Mice; D008815:Mice, Inbred Strains; D019936:Probiotics; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D013045:Species Specificity; D013047:Specific Pathogen-Free Organisms; D018418:Th2 Cells / Q000187:drug effects / Q000276:immunology
D012333:RNA, Messenger; D018664:Interleukin-12; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma