Live and Ultraviolet-Inactivated Lactobacillus Rhamnosus GG Decrease Flagellin-Induced Interleukin-8 Production in Caco-2 Cells  

Oleh:

Lopez, Mariela ; Nan, Li ; Kataria, Jasmeet ; Russell, Michael ; Neu, Josef

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: JN: The Journal of Nutrition vol. 138 no. 11 (Nov. 2008), page 2264.
Topik: Nutritional Immunology

Ketersediaan

Perpustakaan FK Nomor Panggil: J42.K.2008.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Probiotics are widely used in the treatment and prevention of gastrointestinal problems. However, in some immune-compromised populations, the administration of live microorganisms may not be appropriate. A potential alternative to live microorganisms is to inactivate them as long as the beneficial function is retained. We hypothesized that UV-inactivated Lactobacillus rhamnosus GG (LGG) could downregulate interleukin-8 (IL-8) production in intestinal epithelial cells stimulated by the pathogenic ligand, flagellin, using similar mechanisms as live LGG. Caco-2 cells were pretreated with live or UV-inactivated LGG at 1011 colony-forming units/L and stimulated by flagellin at a dose of 500 µg/L. IL-8 production was measured by ELISA, inhibitor of {kappa}B (I{kappa}B) and ubiquitinated-I{kappa}B (Ub-I{kappa}B) expression by immunoblotting and nuclear factor (NF) {kappa}B localization by immunofluorescence staining. Flagellin induced a 17-fold increase in IL-8 production compared with control (P < 0.05), whereas pretreatment with either live LGG or UV-inactivated LGG resulted in 66 and 59% decreases, respectively, compared with the flagellin group (P < 0.05). Flagellin-induced NF{kappa}B nuclear translocation was prevented by both live and UV-inactivated LGG. Flagellin decreased I{kappa}B, which was reversed by either live or UV-inactivated LGG (P < 0.05). UV-inactivated LGG decreased Ub-I{kappa}B expression (P < 0.05), although live LGG had no effect. This study supports the concept that UV-inactivated and live LGG are equally effective in decreasing IL-8 production in the intestinal epithelium. Although the mechanism involves different pathways, both alter cytoplasmic I{kappa}B, thereby inhibiting NF{kappa}B nuclear translocation.

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