Also in lung inflammation alterations in alveolar cell permeability play a role. In experimental studies on mice where lung inflammation was induced by carrageenan disruption of claudin 2, claudin 4 and claudin 5 staining and ZO-1 was observed on cell membranes [15] . Such disruption was partly reversed by blocking TNFα suggesting that TNFα-induced chemotaxis of inflammatory cells might contribute to attenuation of tight junctional permeability in lung inflammation [15] . Additionally, alcohol which provokes patients to lung inflammation and ARDS was shown in experiments on rats to induce changes in claudin expression of alveolar epithelial cells [27] . Chronic alcohol ingestion of rats led to a decrease of claudin 1, 3 and 7 mRNA and protein expression and an increase in claudin 5 mRNA in alveolar epithelial cells resulting in an increased leakiness of tight junctions in the lung [27] . Additionally, inflammatory mediators like IL-1β or IL-6 decrease claudin 3 and 4 levels in amniotic membranes of mice making them more permeable [74] .