This may suggest that exposures that induce TLR5 expression, such as DNA injury, p53 activation (Menendez et al., 2011) or flagellated bacterial infection may in parallel prime the MyD88-dependent pro-inflammatory response to LPS, due to the presence of more TLR5 receptors which may promote TLR4 signaling. This evidence concerns the gene TP53 and bacterial infectious disease.