**8. Inflammation**

Persistent *H. pylori* infection induces chronic inflammation, pro-inflammatory cytokines IL-1, Il-6, IL-8, TNF and micro RNAs, especially those of the let-7 family [95] that correlates significantly with one or various other pro-inflammatory cytokines [96]. Although it would be interesting to determine the role of proinflammatory cytokines in modulating tight junction dysfunction, it is clear that *H. pylori* infection does induce a local inflammatory process by activating nuclear transcription factors NFkB and the chemokine AP-1 [97] where IL-8 enhanced secretion plays an important role [98]. The phosphorylation of the IL-1 receptor after exposure to *H. pylori* reduces the expression of claudin-4 [66]. IL-8 exposure is known to disrupt the organization of epithelial tight junctions leading to "leaky" tight junctions due to a reduced expression of claudin-18 [63].
