Lactobacillus casei MYL01 modulates the proinflammatory state induced by ethanol in an in vitro model
| Autor: | Shiao-Lin Lin, Yi-Heng Chiu, Meei-Yn Lin, Jaw-Ji Tsai |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Lactobacillus casei
medicine.medical_treatment Suppressor of Cytokine Signaling Proteins Biology Microbiology Proinflammatory cytokine Suppressor of Cytokine Signaling 1 Protein Genetics medicine Humans SOCS3 Inflammation Toll-like receptor Ethanol TOLLIP Probiotics Toll-Like Receptors Intracellular Signaling Peptides and Proteins NF-kappa B Hep G2 Cells biology.organism_classification Toll-Like Receptor 2 Cell biology Interleukin-10 Toll-Like Receptor 4 TLR2 Lacticaseibacillus casei Cytokine Toll-Like Receptor 6 Liver Suppressor of Cytokine Signaling 3 Protein Toll-Like Receptor 9 Hepatocytes Animal Science and Zoology RNA Interference Signal transduction Food Science Signal Transduction |
| Zdroj: | Journal of dairy science. 97(4) |
| ISSN: | 1525-3198 |
| Popis: | Accumulating studies have suggested that probiotics have beneficial effects on liver injury but the underlying mechanism has remained unclear. Toll-like receptors (TLR) expressed on immune cells and hepatocytes recognize bacterial components that are translocated from the gut into the portal vein. To date, it has been demonstrated that ethanol alone, without microbial components, is able to activate TLR, leading to promotion of proinflammatory cytokine production. Because the enhanced signaling of TLR triggers persistent inflammation, we hypothesized that development of hepatocyte TLR tolerance to repetitive stimulation plays an important role in protecting the liver from hypergeneration of proinflammatory cytokines. In this study, we showed that Lactobacillus casei MYL01 modulated the proinflammatory state induced by ethanol and investigated in detail the mechanism underlying the observation that L. casei MYL01 gave rise to TLR tolerance toward ethanol stimulation. The effects of L. casei MYL01 in the attenuation of ethanol-induced liver damage were due to enhancement of IL-10 production, which limited the proinflammatory process. Furthermore, better defense of hepatocytes against ethanol challenge by treatment of L. casei MYL01 was attributed to previous induction of toll interacting protein (TOLLIP) and suppressor of cytokine signaling (SOCS)1 and SOCS3 expression via activation of TLR1, TLR2, TLR6, and TLR9, an action that cross-regulated ethanol-TLR4-nuclear factor κB signal transduction events. This finding might help establish an in vitro platform for selecting hepatoprotective probiotic strains in terms of ethanol-induced liver damage. |
| Databáze: | OpenAIRE |
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