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. 2014 Nov 3;9(11):e111460. doi: 10.1371/journal.pone.0111460

Figure 3. TLR4 Asp299Gly and Thr399Ile polymorphisms have dysregulated LPS-induced TLR4 signalling.

Figure 3

(A and B) TLR4 polymorphisms affect gene expression in both the MyD88 dependent and independent signalling pathways. NF-κB and IFN-B gene expression following E. coli LPS stimulation (1 µg/ml) depicted as fold change after normalisation to unstimulated values. Graphical representation reflects fold change difference between median values from wildtype and TLR4 polymorphic carriers. Error bars  =  Standard error. (C) TLR4 polymorphisms inhibit p65-phosphorylation Human PBMCs were incubated with or without E. coli LPS (1 µg/ml) upto 30 mins (15 min LPS stimulation depicted) and then analysed for the distribution of p65 by immunofluorescence. Red stain indicates the localization of p65, and blue stain indicates the nucleus (magnification, 200x). Mean percentage of NF-κB translocation in peripheral blood derived monocytes from wildtype individuals and carriers of the TLR4 Asp299Gly polymorphism. Data generated from 3 individuals per group tested in 3 separate experiments. *T-test statistic for comparison at each time point between wildtype and TLR4 variant carriers. (D) TLR4 polymorphisms affect downstream cytokine production. Box-and-whisker plots of cytokine production by monocytes from wildtype and TLR4 Asp299Gly and Thr399Ile polymorphic carriers stimulated with E. coli LPS (1 µg/ml) for 24 h. The bold lines represent medians, and the span of the box represents the interquartile range of the data, * depicts outliers. Data is generated from sample groups of 10 volunteers.