The Immunologically Active Oligosaccharides Isolated from Wheatgrass Modulate Monocytes via Toll-like Receptor-2 Signaling

Tsai, Chia-Che; Lin, Chih-Ru; Tsai, Hsien-Yu; Chen, Chia‐Jung; Li, Wen‐Tai; Yu, Hon‐Tsen; Ke, Yi‐Yu; Hsieh, Wei-Ying; Chang, Chung‐Che; Wu, Chung‐Yi; Chen, Shui‐Tein; Wong, Chi‐Huey

doi:10.1074/jbc.m112.448381

Cited by 32 publications

(18 citation statements)

References 31 publications

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“…Taken together, these results support a view that prebiotics may be directly activating TLR signaling to alter cytokine/chemokine expressions and the integrity of the epithelial barrier. This is also in line with multiple reports showing that prebiotics induce cytokine and chemokine production in monocytes and intestinal epithelial cells in a TLR2- or TLR4-dependent fashion121928293031. However, whether PKCδ is the only PKC isoform or the only signal transduction pathway affected is still unclear.…”

Section: Discussionsupporting

confidence: 89%

Protein kinase C δ signaling is required for dietary prebiotic-induced strengthening of intestinal epithelial barrier function

Abdullah

Määttänen

et al. 2017

Sci Rep

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Prebiotics are non-digestible oligosaccharides that promote the growth of beneficial gut microbes, but it is unclear whether they also have direct effects on the intestinal mucosal barrier. Here we demonstrate two commercial prebiotics, inulin and short-chain fructo-oligosaccharide (scFOS), when applied onto intestinal epithelia in the absence of microbes, directly promote barrier integrity to prevent pathogen-induced barrier disruptions. We further show that these effects involve the induction of select tight junction (TJ) proteins through a protein kinase C (PKC) δ-dependent mechanism. These results suggest that in the absence of microbiota, prebiotics can directly exert barrier protective effects by activating host cell signaling in the intestinal epithelium, which represents a novel alternative mechanism of action of prebiotics.

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Section: Discussionsupporting

confidence: 89%

Protein kinase C δ signaling is required for dietary prebiotic-induced strengthening of intestinal epithelial barrier function

Abdullah

Määttänen

et al. 2017

Sci Rep

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“…Although it has been described that TLR stimulation modulates the expression of the CD80 and CD86 costimulatory markers on monocytes [25], little is known about the role of HIV-1 infection on the modulation of the expression of both markers on monocytes CD14+ in the presence of TLR agonists. Therefore, we investigated whether expression of these two markers is affected by HIV-1 in the presence of Pam 3 CSK 4 , LPS or CpG-B ODN; cells stimulated only with TLR agonists served as controls.…”

Section: Resultsmentioning

confidence: 99%

Impact of in vitro Costimulation with TLR2, TLR4 and TLR9 Agonists and HIV-1 on Antigen-Presenting Cell Activation

2015

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Objective: HIV-1 infects several immune cells including dendritic cells (DCs) and monocytes, which contributes in both to dissemination of HIV-1 infection and induction of antiviral immunity. These cells produce high amounts of type I IFN and proinflammatory cytokines upon Toll-like receptor (TLR) stimulation. During HIV-1 infection, an altered production of proinflammatory cytokines has been reported. However, the mechanisms underlying cytokine modulation have not been well described. Here, we evaluated the production of proinflammatory cytokines and activation of myeloid and plasmacytoid DCs and monocytes costimulated in vitro with TLR agonists and HIV-1. Methods: Changes in cytokine expression by real-time PCR and activation of DCs and monocytes by flow cytometry were evaluated after costimulation with HIV-1 and TLR agonists. Results: We observed an upregulation of TNF-α expression after TLR4 stimulation, but a downregulation of IL-6 when TLR2/TLR9 were stimulated. Interestingly, the expression of CD80 and CD86 costimulatory molecules in monocytes and DCs were significantly increased in cells challenged with HIV-1 and TLR2/TLR4/TLR9 agonists. Conclusion: This regulation of TNF-α and IL-6 production and changes in the expression of costimulatory molecules can be critical in the context of HIV-1 infection, by favoring the antigen-presenting cell activation through the stimulation of TLRs.

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“…2B). As TLR2 and TRL4 are important TLRs which recognise dietary carbohydrate oligomers and polymers (Capitan-Canadas et al, 2014;Kim, Muto, & Gallo, 2013;Lin et al, 2014a;Tsai et al, 2013;Vogt et al, 2013), we investigated whether NF-κB activation by cellulose was mediated via TLR2 or TLR4. To this end, HEK-Blue TLR reporter cells with individual TLR constructs were stimulated with cellulose.…”

Section: Cellulose Activates Nuclear Factor Kappa B Via Toll-like Recmentioning

confidence: 99%

Cellulose alters the expression of nuclear factor kappa B-related genes and Toll-like receptor-related genes in human peripheral blood mononuclear cells

Vogt

Boekschoten

Groot

et al. 2015

Journal of Functional Foods

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The Immunologically Active Oligosaccharides Isolated from Wheatgrass Modulate Monocytes via Toll-like Receptor-2 Signaling

Cited by 32 publications

References 31 publications

Protein kinase C δ signaling is required for dietary prebiotic-induced strengthening of intestinal epithelial barrier function

Protein kinase C δ signaling is required for dietary prebiotic-induced strengthening of intestinal epithelial barrier function

Impact of in vitro Costimulation with TLR2, TLR4 and TLR9 Agonists and HIV-1 on Antigen-Presenting Cell Activation

Cellulose alters the expression of nuclear factor kappa B-related genes and Toll-like receptor-related genes in human peripheral blood mononuclear cells

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