Tight junctions are important for lung defense since they function as a barrier for pathogens and other exogenous compounds preventing their penetration into the interstitial tissues. Tight junctions may thus be considered as a part of the innate immune system. The epithelial barriers of bronchi are, however, relatively leaky with a comparatively low transmembrane resistance of approximately 100 Ωcm2 compared to endothelial cell junctions of the blood brain barrier which have a 1500-2000 Ωcm2 barrier resistance [14, 35] . The thickness of the tight junctional belt in airway epithelia varies from 0.27 μm to 0.37 μm depending on the cell type [36] . There are reports of fragmentation and thinning of the tight junctional belt in diseases such as asthma and focal proliferations and thinnings are described in lung neoplasia such as bronchioloalveolar carcinoma [36] . Such changes are also seen in cell line studies induced by cytokines [37] Lungs are exposed to several pathogens and noxious stimuli which may influence paracellular permeability of bronchial airways, alveolar cells or endothelial barriers in alveolar walls. Tobacco smoke makes tight junctions leakier [36] . Carcinogenic compounds such as bentzpyrene and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) influence claudin synthesis by upregulating transcription factors like twist, snail or ZEB1 [38, 39] resulting in downregulation of E-cadherin and claudins. Exposure of lung BEAS-2B cells and cancer cell lines to tobacco smoke leads to changes in claudin expression [40] . In bronchial cells sampled from smoking COPD patients and healthy smokers claudins and other tight junction genes are downregulated [41] . Tobacco smoke also induces the formation of reactive oxygen species. In kidney epithelial MDCK (Madine-Darby canine kidney strain) II cells, exposure to hydrogen peroxide leads to bimodal changes in the transepithelial barrier permeability with activation of ERK1/2 and p38 kinases, and a decrease in occludin, claudin 1 and claudin 2 levels [42] . Such changes could also make the bronchial and alveolar epithelium leakier and the airways more vulnerable to damage caused by pathogens causing irritation and chronic infection. On the other hand, an increase in claudin 2 expression leads to lower transepithelial resistance in MDCK I and II cells and formation of paracellular water channels [43, 44] . Generally air pollutants influence the barrier function of airway epithelium. Particulate matter of less than 10 μm in diameter decreases the transepithelial potential in airway epithelial cells causing internalization of occludin and its dissociation from ZO-1 [45] .