**7. Lipopolysaccharide**

Gut bacterial lipopolysaccharides (LPS) are known to affect intracellular signaling as well as tight junctions of the blood brain barrier [87] and the intestinal barrier [88]. LPS, an important structural component of bacterial walls' outer membrane, is recognized by the membrane toll-like receptor 4, and alterations in permeability induced by LPS are via a TLR-4 dependent process associated to the adaptor protein focal adhesion kinase, which has been shown to co-localize with claudin-1 [89], and the activation of the MyD88-dependent pathway [90]. *H. pylori* LPS has an agonist function upon TLR-2 and not TLR-4 [91, 92]. We have shown that *H. pylori* LPS induces the expression of TLR-2 and that the greater expression of the receptor was accompanied by an initial increase in claudin-4 followed by claudin-6, −7 and − 9; this initial process was STAT3-dependent whereas the expression of claudin-6, −7 and − 9 was ERK1/2-dependent (**Figure 5**) [93]. The same pathway has been reported in claudin-1 downregulation in keratinocytes [94].
