Campylobacter jejuni activates NF-κB independently of TLR2, TLR4, Nod1 and Nod2 receptors
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- 作者：Abdullah F. Al-Sayeqh ; Michael F. Loughlin ; Eleanor Dillon ; Kenneth H. Mellits ; Ian F. Connerton
- 关键词：Campylobacter jejuni ; NF-κ ; B activation ; TLR ; Nod
- 刊名：Microbial Pathogenesis
- 出版年：2010
- 出版时间：November 2010
- 年：2010
- 卷：49
- 期：5
- 页码：294-304
- 全文大小：323 K
文摘
Campylobacter jejuni activates the host transcription factor NF-κB that regulates the expression of a number of genes involved in the inflammatory response to bacterial infection. Signaling pathways leading to NF-κB by pathogens and/or their products include transmembrane Toll-like receptors (TLRs) and intracellular receptors nucleotide-binding oligomerization domain proteins (Nods). This study was carried out to investigate the role of TLRs (TLR2 and TLR4) and Nods (Nod1 and Nod2) receptors in mediating NF-κB activation by C. jejuni. By means of transfecting receptors/molecules under study and measuring reporter gene activity, NF-κB activation and subsequent cytokine production by live, heat-killed C. jejuni, or boiled cell extract (BCE) were observed in a range of tissue culture cell lines. This activation is reduced upon transfection of cells with the dominant negative versions (DNV) of TLR-adaptor molecule MyD88. NF-κB activation was observed to be augmented in cell lines transfected with TLR2, Nod1, and Nod2 but not with TLR4. Additionally, NF-κB activation by C. jejuni was observed to be independent of Nod1 and Nod2 in cells transfected with DNV of these receptors. NF-κB activation pathway by C. jejuni may represent a novel mechanism utilising unknown receptors up-regulated by yet to be characterized active component(s). To our knowledge, such observations have not been previously reported for C. jejuni or any other food-borne pathogen.