The permeability of tight junctions in epithelia is an important factor in several pulmonary diseases. Pathogens causing infections are many some of which may act by downregulating claudins or causing their deranged distribution inducing changes in tight junctional permeability allowing pathogens to invade through epithelial barriers. In lung disease the effect of such pathogens on claudin expression or cellular distribution is still mainly unelucidated and needs further research. Alteration of claudin expression also plays an important role in lung diseases such as COPD, asthma, and ARDS. Influencing alveolar or endothelial permeability by manipulation the expression of claudins (eg. claudins 4 and 5) might be future targets in the treatment of lung injury. Changes in the expression of claudins are also seen in pulmonary neoplasia reflecting complex changes in several genes related to tumor growth, spread and differentiation producing a characteristic expression patterns in histologically different tumor types. In adenocarcinomas a proposed new classification will surely also change our perspectives on assessment of claudins on the behavior of these tumors [113] . In addition to claudin 3 and 4 which may have therapeutic implications for tumor treatment in the future, claudin 18 might also be a new target for antibody mediated therapy in lung cancer [114] .