Oral administration of Lactococcus chungangensis inhibits 2,4-dinitrochlorobenzene-induced atopic-like dermatitis in NC/Nga mice.
Interest is increasing in the potentially beneficial role of probiotics in the prevention and treatment of atopic diseases. In this study, we investigated the protective effects of Lactococcus chungangensis CAU 28(T) against atopic dermatitis using murine macrophage RAW 264.7 cells, human keratinocyte HaCaT cells, human mast cell line HMC-1 cells, and a 2,4-dinitrochlorobenzene-induced atopic dermatitis model (NC/Nga mice). The results showed that L. chungangensis CAU 28(T) exhibited potent antiinflammatory activity by inhibiting the production of the proinflammatory mediators nitric oxide and prostaglandin E2 in lipopolysaccharide-stimulated RAW 264.7 cells. Treatment with L. chungangensis CAU 28(T) reduced the release of β-hexosaminidase and histamine in HMC-1 cells stimulated with mast cell activator compound 48/80. In addition, the back skin and ears of NC/Nga mice exhibited reduced histological manifestations of atopic skin lesions such as erosion, hyperplasia of the epidermis and dermis, and inflammatory cell infiltration. Oral administration of L. chungangensis CAU 28(T) suppressed the production of IL-4, IL-5, IL-12, IFN-γ, tumor necrosis factor-α, and thymus- and activation-regulated chemokine (TARC) in skin lesions, indicating that it strongly drives the local immune system with efficacy comparable to that of tacrolimus, a topical immunomodulatory drug used for the treatment of atopic dermatitis. The findings indicate that L. chungangensis CAU 28(T) could be a novel probiotic candidate for controlling the symptoms of atopic dermatitis.
Department of Microbiology, Chung-Ang University College of Medicine, 84 Heukseok-ro, Dongjak-gu, Seoul 06974, Republic of Korea.
Woo Jin
WJ
Choi
Department of Microbiology, Chung-Ang University College of Medicine, 84 Heukseok-ro, Dongjak-gu, Seoul 06974, Republic of Korea.
Maytiya
M
Konkit
Department of Microbiology, Chung-Ang University College of Medicine, 84 Heukseok-ro, Dongjak-gu, Seoul 06974, Republic of Korea.
Yena
Y
Kim
Department of Pathology, Chung-Ang University College of Medicine, 84 Heukseok-ro, Dongjak-gu, Seoul 06974, Republic of Korea.
Mi-Kyung
MK
Kim
Department of Microbiology, Chung-Ang University College of Medicine, 84 Heukseok-ro, Dongjak-gu, Seoul 06974, Republic of Korea. Electronic address: kimwy@cau.ac.kr.
Wonyong
W
Kim
D000284:Administration, Oral; D000818:Animals; D045744:Cell Line, Tumor; D002470:Cell Survival; D054414:Chemokine CCL17 / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000139:chemically induced / Q000628:therapy*; D004137:Dinitrochlorobenzene / Q000633:toxicity*; D015232:Dinoprostone / Q000378:metabolism; D005260:Female; D006632:Histamine / Q000378:metabolism; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007371:Interferon-gamma / Q000378:metabolism; D018664:Interleukin-12 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D017045:Lactococcus; D008070:Lipopolysaccharides / Q000633:toxicity; D008407:Mast Cells / Q000382:microbiology; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism; D019936:Probiotics / Q000008:administration & dosage*; D000067996:RAW 264.7 Cells; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012867:Skin / Q000382:microbiology / Q000473:pathology; D016559:Tacrolimus / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000378:metabolism; D001619:beta-N-Acetylhexosaminidases / Q000378:metabolism
C499538:Ccl17 protein, mouse; D054414:Chemokine CCL17; D004137:Dinitrochlorobenzene; D015848:Interleukin-5; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D018664:Interleukin-12; D015847:Interleukin-4; D009569:Nitric Oxide; D007073:Immunoglobulin E; D006632:Histamine; D007371:Interferon-gamma; D001619:beta-N-Acetylhexosaminidases; D015232:Dinoprostone; D016559:Tacrolimus
Lactococcus; anti-atopic dermatitis; antiallergy; antiinflammatory