Interestingly, protein kinase C delta inhibitor appeared to inhibit sepsis induced lung injury, such as disruption of lung tissue or development of edema [72] . In nasal epithelial cells treatment of cells with protein kinase C activator 12-O-tetradecanoylophospho-13-acetate led to an increased transepithelial electrical resistance and upregulation of claudin 1, ZO1, ZO2 and occludin [73] . It was shown that the upregulation of the tight junctional proteins was due to activation of PKC lambda and theta partly induced by the transcription factor GATA 3 [73] . In fact, phosphorylation of threonine sites in claudins by PKC or PKA may dislocate claudins from cellular membranes resulting in changed tight junctional properties [1] .