Administration of Lactococcus lactis strain Plasma induces maturation of plasmacytoid dendritic cells and protection from rotavirus infection in suckling mice

2018 ◽  
Vol 56 ◽  
pp. 205-211 ◽  
Author(s):  
Kenta Jounai ◽  
Tetsu Sugimura ◽  
Yuji Morita ◽  
Konomi Ohshio ◽  
Daisuke Fujiwara
Keyword(s):  
Dendritic Cells ◽  
Lactococcus Lactis ◽  
Plasmacytoid Dendritic Cells ◽  
Rotavirus Infection ◽  
Suckling Mice ◽  
Lactis Strain

scholarly journals Effect of Lactococcus lactis Strain Plasma on HHV-6 and HHV-7 Shedding in Saliva: A Prospective Observational Study

2021 ◽  
Vol 9 (8) ◽  
pp. 1683
Author(s):  
Hiroki Miura ◽  
Masaru Ihira ◽  
Kei Kozawa ◽  
Yoshiki Kawamura ◽  
Yuki Higashimoto ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Salivary Gland ◽  
Observational Study ◽  
Lactococcus Lactis ◽  
Prospective Observational Study ◽  
Viral Dna ◽  
Younger Adults ◽  
Lactis Strain ◽  
Study Participants ◽  
Second Period

HHV-6 and HHV-7 can reactivate in the salivary gland in response to various host stresses. Lactococcus lactis strain Plasma (LC-Plasma) can activate plasmacytoid dendritic cells (pDCs) and decrease viral infection. We investigated whether LC-Plasma intake could decrease HHV-6 and HHV-7 reactivation in the salivary gland. A total of 54 healthy volunteers were enrolled in this study. Participants took LC-Plasma granules daily for 6 weeks. Saliva samples were collected from subjects weekly for 4 weeks before (first), during (second), and after (third period) LC-Plasma intake. There was a 2-week interval between the first and second periods and a 3-week interval between the second and third periods. Mean salivary HHV-6 and HHV-7 DNA loads were compared among the three observation periods. In the first period (baseline data of viral DNA shedding), HHV-6 DNA shedding was significantly higher in subjects under 40 years old, and HHV-7 DNA shedding was significantly higher in males. HHV-6 and HHV-7 DNA loads did not significantly differ between periods. Meanwhile, in a subgroup analysis of the subjects under 40 years old, HHV-6 DNA load was significantly lower in the second period than in the first period. LC-Plasma decreases HHV-6 reactivation in the salivary glands in younger adults.

Immunomodulatory effect of Lactococcus lactis JCM5805 on human plasmacytoid dendritic cells

2013 ◽  
Vol 149 (3) ◽  
pp. 509-518 ◽  
Author(s):  
Tetsu Sugimura ◽  
Kenta Jounai ◽  
Konomi Ohshio ◽  
Takaaki Tanaka ◽  
Masahiro Suwa ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Lactococcus Lactis ◽  
Plasmacytoid Dendritic Cells ◽  
Immunomodulatory Effect

Staphylococcus aureus Epicutaneous Infection Is Suppressed by Lactococcus lactis Strain Plasma via Interleukin 17A Elicitation

2019 ◽  
Vol 220 (5) ◽  
pp. 892-901
Author(s):  
Ryohei Tsuji ◽  
Toshio Fujii ◽  
Yuumi Nakamura ◽  
Kamiyu Yazawa ◽  
Osamu Kanauchi
Keyword(s):  
Staphylococcus Aureus ◽  
Dendritic Cells ◽  
Oral Administration ◽  
Lactococcus Lactis ◽  
Skin Inflammation ◽  
Type I ◽  
Interleukin 17A ◽  
Skin Immunity ◽  
Lactis Strain

AbstractBackgroundLactococcus lactis strain Plasma (LC-Plasma) was revealed to stimulate plasmacytoid dendritic cells and induce antiviral immunity in vitro and in vivo. In this study, we assessed the effects of LC-Plasma on skin immunity.MethodsTo evaluate the effect of LC-Plasma on skin immunity and Staphylococcus aureus epicutaneous infection, lymphocyte activities in skin-draining lymph nodes (SLNs) and gene expression in skin were analyzed after 2 weeks of oral administration of LC-Plasma. To evaluate the mechanisms of interleukin 17A production, SLN lymphocytes were cultured with or without LC-Plasma, and the interleukin 17A concentrations in supernatants were measured.ResultsOral administration of LC-Plasma activated plasma dendritic cells in SLNs, augmented skin homeostasis, and elicited suppression of Staphylococcus aureus, Staphylococcus epidermidis, and Propionibacterium acnes proliferation. In addition, significant suppression of the S. aureus burden and reduced skin inflammation were observed following oral administration of LC-Plasma. Furthermore, a subsequent in vitro study revealed that LC-Plasma could elicit interleukin 17A production from CD8+ T cells and that its induction mechanism depended on the Toll-like receptor 9 signaling pathway, with type I interferon partially involved.ConclusionsOur results suggest that LC-Plasma oral administration enhances skin homeostasis via plasma dendritic cell activation in SLNs, resulting in suppression of S. aureus epicutaneous infection and skin inflammation.

Erratum to “Immunomodulatory effect of Lactococcus lactis JCM5805 on human plasmacytoid dendritic cells” [Clin. Immunol. 149 (2013) 509-518]

2015 ◽  
Vol 161 (2) ◽  
pp. 156
Author(s):  
Tetsu Sugimura ◽  
Kenta Jounai ◽  
Konomi Ohshio ◽  
Takaaki Tanaka ◽  
Masahiro Suwa ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Lactococcus Lactis ◽  
Plasmacytoid Dendritic Cells ◽  
Immunomodulatory Effect

PLASMACYTOID DENDRITIC CELLS FUNCTION IN HIV INFECTION

2008 ◽  
Vol 31 (4) ◽  
pp. 13
Author(s):  
Martin Hyrcza ◽  
Mario Ostrowski ◽  
Sandy Der
Keyword(s):  
Dendritic Cells ◽  
Influenza Virus ◽  
Hiv Infection ◽  
Gene Transcription ◽  
Sendai Virus ◽  
Plasmacytoid Dendritic Cells ◽  
Type I Interferons ◽  
Interferon Response ◽  
Type I ◽  
Type I Ifn

Plasmacytoid dendritic cells (pDCs) are innate immune cells able to produce large quantities of type I interferons (IFN) when activated. Human immunodeficiency virus (HIV)-infected patients show generalized immune dysfunction characterized in part by chronic interferon response. In this study we investigated the role of dendritic cells inactivating and maintaining this response. Specifically we compared the IFN geneactivity in pDCs in response to several viruses and TLR agonists. We hypothesized that 1) the pattern of IFN gene transcription would differ in pDCs treated with HIV than with other agents, and 2) that pDCs from patients from different stages of disease would respond differently to the stimulations. To test these hypotheses, we obtained pDCs from 15 HIV-infected and uninfected individuals and treated freshly isolated pDCs with either HIV (BAL strain), influenza virus (A/PR/8/34), Sendai virus (Cantell strain), TLR7 agonist(imiquimod), or TLR9 agonist (CpG-ODN) for 6h. Type I IFN gene transcription was monitored by real time qPCRfor IFNA1, A2, A5, A6, A8,A17, B1, and E1, and cytokine levels were assayed by Cytometric Bead Arrays forTNF?, IL6, IL8, IL10, IL1?, and IL12p70. pDC function as determined by these two assays showed no difference between HIV-infected and uninfected patients or between patients with early or chronic infection. Specifically, HIV did notinduce type I IFN gene expression, whereas influenza virus, Sendai virus and imiquimod did. Similarly, HIV failed to induce any cytokine release from pDCs in contrast to influenza virus, Sendai virus and imiquimod, which stimulatedrelease of TNF?, IL6, or IL8. Together these results suggest that the reaction of pDCs to HIV virus is quantitatively different from the response to agents such as virus, Sendai virus, and imiquimod. In addition, pDCs from HIV-infected persons have responses similar to pDCs from uninfected donors, suggesting, that the DC function may not be affected by HIV infection.

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