In this setting, lipopolysaccharide (LPS), a cell wall constituent of Gram- bacteria, crucial in maintaining the integrity and viability of bacterial cells, has been studied as involved in the modulation of susceptibility to inflammation in patients with GERD through the interaction with toll-like receptors 4 (TLR-4) and the subsequent activation of the innate immune system [47], as shown in in vitro and in vivo studies [51], [52]. Here, TLR4 is linked to gastroesophageal reflux disease.