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Lipopolysaccharide (LPS) is a major integral component of the outer membrane of Gram-negative bacteria cell walls, that is released when bacteria lyse. LPS was shown to stimulate immune system cells by binding the cell-surface Toll-like receptor 4 (TLR4) and activating transcription factors and protein kinases, such as NF-kB and p38 kinase. This in turn was shown to result in an increased production of proinflammatory cytokines and overexpression of cell adhesion molecules and matrix-degrading enzymes.1 The pathogenic role of LPS has been shown to be linked to several disease-states, viz., liver diseases, neurological degeneration, chronic inflammation of the gut, diabetes, and prostate cancer metastasis.2–4 One of our pioneering works5 showed increased circulatory levels of LPS and Zonulin as novel biomarkers of proinflammation in patients with type 2 diabetes. LPS is also proatherogenic factor and apart from its increase in blood levels in patients with atherosclerosis, LPS from Escherichia coli has also been shown to localize in carotid plaques, implying a mediatory role in atherosclerotic lesions.6

LPS—Is It a Major Liability Factor for Cancer Risk and Severity?