Clostridium butyricum activates TLR2-mediated MyD88-independent signaling pathway in HT-29 cells
2011-10-301497
Abstract
Oral administration of Clostridium butyricum as probiotic is increasingly gaining importance in the treatmentof diarrhea and the improvement of animal performance. However, the mechanisms of host cell receptorrecognition of C. butyricum and the downstream immune signaling pathways leading to these benefits remainunclear. The objective of this study was to analyze the mechanisms involved in C. butyricum induction ofthe toll-like receptor (TLR) signaling. Knockdown of myeloid differentiation primary response protein 88(MyD88) expression using small interfering RNA in this manner did not affect C. butyricum -induced elevatedlevels of nuclear factor κB (NF-κB), interleukin-8 (IL-8), IL-6, and tumor necrosis factor alpha (TNF-α),suggesting a MyD88-independent route to TLR signaling transduction. However, a significant reduction inthe levels of NF-κB, IL-8, IL-6, and TNF-α was evident in the absence of TLR2 expression, implying theneed for TLR2 inC.butyricum recognition. Hence, C. butyricum activates TLR2-mediated MyD88-independent signaling pathway in human epithelial cells, which adds to our understanding of the molecularmechanisms of this probiotic action on gut epithelium.
Keywords Clostridium butyricum - TLR2 - MyD88 - NF-κB - HT-29 cells
Oral administration of Clostridium butyricum as probiotic is increasingly gaining importance in the treatmentof diarrhea and the improvement of animal performance. However, the mechanisms of host cell receptorrecognition of C. butyricum and the downstream immune signaling pathways leading to these benefits remainunclear. The objective of this study was to analyze the mechanisms involved in C. butyricum induction ofthe toll-like receptor (TLR) signaling. Knockdown of myeloid differentiation primary response protein 88(MyD88) expression using small interfering RNA in this manner did not affect C. butyricum -induced elevatedlevels of nuclear factor κB (NF-κB), interleukin-8 (IL-8), IL-6, and tumor necrosis factor alpha (TNF-α),suggesting a MyD88-independent route to TLR signaling transduction. However, a significant reduction inthe levels of NF-κB, IL-8, IL-6, and TNF-α was evident in the absence of TLR2 expression, implying theneed for TLR2 inC.butyricum recognition. Hence, C. butyricum activates TLR2-mediated MyD88-independent signaling pathway in human epithelial cells, which adds to our understanding of the molecularmechanisms of this probiotic action on gut epithelium.
Keywords Clostridium butyricum - TLR2 - MyD88 - NF-κB - HT-29 cells
