Inflammatory immune activation is observed in patients with chronic heart failure (CHF). LPS translocated from the intestine into circulation during episodes of decompensation can modulate the activation of immunocompetent cells in patients with CHF. The expression of transcriptional nuclear factor kappa-B (NF-κB) in patients with CHF was significantly highest than control subject. Subsequently in vitro stimulation of peripheral blood mononuclear cells (PBMC) with lipopolysaccharide (LPS) did not induce NF-κB nuclear translocation in cells from patients with CHF with NYHA II-IV as compared to the cells from healthy patients with LPS induction. This phenomenon of “LPS- tolerance” or “deactivation” can explain the endotoxin hypothesis, which suggests that bacterial translocation through the oedematous gut wall with subsequent release of endotoxin may pose the relevant stimulus to trigger NF-κB system.