Lactobacillus plantarum L-137 upregulates hyaluronic acid production in epidermal cells and fibroblasts in mice

Heat-killed Lactobacillus plantarum L-137 (HK L-137), an immunobiotic lactic acid bacterium, has been reported to enhance IFN-γ production through induction of IL-12. In this study, we investigated the effects of HK L-137 on skin moisturizing and production of hyaluronic acid (HA), an extracellular...

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Published inMicrobiology and immunology Vol. 63; no. 9; p. 367
Main Authors Nakai, Hiroko, Hirose, Yoshitaka, Murosaki, Shinji, Yoshikai, Yasunobu
Format Journal Article
LanguageEnglish
Published Australia 01.09.2019
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Abstract Heat-killed Lactobacillus plantarum L-137 (HK L-137), an immunobiotic lactic acid bacterium, has been reported to enhance IFN-γ production through induction of IL-12. In this study, we investigated the effects of HK L-137 on skin moisturizing and production of hyaluronic acid (HA), an extracellular matrix associated with the retention of skin moisture. Oral administration of HK L-137 suppressed the loss of water content in the stratum corneum in hairless mice. Treatment of primary epidermal cells with HK L-137 increased HA production. Supernatant from immune cells stimulated by HK L-137, which contained proinflammatory cytokines such as IL-12, TNF-α, and IFN-γ, upregulated HA production and hyaluronan synthase 2 (HAS2) messenger RNA expression by BALB/3T3 fibroblasts via activation of transcription factor nuclear factor κB (NFκB). Although treatment of the supernatant with anti-TNF-α antibody (Ab) alone did not inhibit the HA production, combination of anti-TNF-α Ab with anti-IFN-γ Ab significantly inhibited the HA production. Thus, HK L-137-induced IFN-γ plays a critical role in upregulated HA production in collaboration with TNF-α. HK L-137 may be useful for improvement of skin functions such as moisture retention by inducing HA production.
AbstractList Heat-killed Lactobacillus plantarum L-137 (HK L-137), an immunobiotic lactic acid bacterium, has been reported to enhance IFN-γ production through induction of IL-12. In this study, we investigated the effects of HK L-137 on skin moisturizing and production of hyaluronic acid (HA), an extracellular matrix associated with the retention of skin moisture. Oral administration of HK L-137 suppressed the loss of water content in the stratum corneum in hairless mice. Treatment of primary epidermal cells with HK L-137 increased HA production. Supernatant from immune cells stimulated by HK L-137, which contained proinflammatory cytokines such as IL-12, TNF-α, and IFN-γ, upregulated HA production and hyaluronan synthase 2 (HAS2) messenger RNA expression by BALB/3T3 fibroblasts via activation of transcription factor nuclear factor κB (NFκB). Although treatment of the supernatant with anti-TNF-α antibody (Ab) alone did not inhibit the HA production, combination of anti-TNF-α Ab with anti-IFN-γ Ab significantly inhibited the HA production. Thus, HK L-137-induced IFN-γ plays a critical role in upregulated HA production in collaboration with TNF-α. HK L-137 may be useful for improvement of skin functions such as moisture retention by inducing HA production.
Author Murosaki, Shinji
Yoshikai, Yasunobu
Nakai, Hiroko
Hirose, Yoshitaka
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Issue 9
Keywords skin
IFN-γ
Lactobacillus plantarum L-137
hyaluronic acid
Language English
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Snippet Heat-killed Lactobacillus plantarum L-137 (HK L-137), an immunobiotic lactic acid bacterium, has been reported to enhance IFN-γ production through induction of...
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StartPage 367
SubjectTerms Animals
BALB 3T3 Cells
Cytokines - metabolism
Epidermal Cells - metabolism
Epidermal Growth Factor - metabolism
Female
Fibroblasts - metabolism
Hyaluronan Synthases
Hyaluronic Acid - metabolism
Interferon-gamma - metabolism
Interleukin-12 - metabolism
Lactobacillus plantarum - physiology
Mice
Mice, Inbred BALB C
RNA, Messenger - metabolism
Skin
Spleen
Tumor Necrosis Factor-alpha - metabolism
Up-Regulation - drug effects
Title Lactobacillus plantarum L-137 upregulates hyaluronic acid production in epidermal cells and fibroblasts in mice
URI https://www.ncbi.nlm.nih.gov/pubmed/31273816
Volume 63
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