Alive and Dead Lactobacillus rhamnosus GG Decrease Tumor Necrosis Factor-[alpha]-Induced Interleukin-8 Production in Caco-2 Cells
2005
Zhang, Liyan | Li, Nan | Caicedo, R (Ricardo) | Neu, Josef
Certain probiotic bacteria show anti-inflammatory activity after being heat killed, whereas others do not, suggesting that the gastrointestinal environment may alter the activity of probiotic bacteria. Occasionally, probiotics are provided when a patient is also being treated with oral antibiotics; this may have an effect on the probiotic activity. We hypothesized that Lactobacillus rhamnosus GG (LGG) are capable of downregulating tumor necrosis factor-[alpha] (TNF[alpha])-induced interleukin (IL)-8 production under all 3 of these conditions, and that LGG act through the nuclear factor [kappa]B (NF[kappa]B)/inhibitor of [kappa]B (I[kappa]B) pathway. Caco-2 cells were treated with live or heat-killed LGG in doses ranging from 10⁴ to 10¹⁰ cfu/L, in the presence or absence of antibiotics and TNF[alpha] in the media. TNF[alpha]-induced production of IL-8 by Caco-2 cells was modulated by LGG under all 3 conditions. However, higher doses of live LGG without TNF[alpha] in the presence or absence of antibiotics in vitro induced the production of IL-8 (P = 0.001). Heat-killed LGG also blunted the TNF[alpha]-induced IL-8 production (P < 0.01), but by itself did not increase IL-8 production at higher doses as markedly as live LGG (P < 0.05). LGG reduced the TNF[alpha]-induced NF[kappa]B translocation to the nucleus and lessened the decrease in I[kappa]B in the cytoplasm (P < 0.05). LGG reduced TNF[alpha]-induced IL-8 production by affecting the NF[kappa]B/I[kappa]B pathway in Caco-2 cells. High doses of live LGG markedly increased IL-8 production, but heat-killed LGG caused only a slight increase in IL-8. Thus, heat-killed LGG may effectively ameliorate inflammation with a lower potential than live LGG at high doses to cause inflammation.
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