Mechanisms of pathogen entry and its association with claudins have not been so extensively studied in the respiratory tract. It, however, appears probable that similar mechanisms apply to airway epithelia. Matrix metalloproteinase 9 (MMP 9)decreases epithelial barrier function in bronchial cells, and increases their vulnerability to adenovirus infection [65] . The cells show disruption of regular membranous staining pattern of claudin 1 and occludin and internalization of reactivity following MMP9 treatment which could be restored by tissue inhibitor of matrix metalloproteinase 1 (TIMP1) [65] . Pseudomonas aeruginosa has been shown to invade airway epithelial barriers by destroying tight junctions [66] . Interestingly, Plasmodium falciparum malaria affects lung endothelial cells by relocation of ZO-1 from the plasma membrane and downregulation of claudin 5 [67] . Thus also parasite infections may be associated with tight junctional changes in the pulmonary cells.