Regulation of the metal transport protein DMT1 may contribute to the uptake and detoxification of iron by cells resident in the respiratory tract. Inflammation has been associated with an increased availability of this metal resulting in an oxidative stress. Because pro-inflammatory cytokines and lipopolysaccharide (LPS) have been demonstrated to affect an elevated expression of DMT1 in a macrophage cell line, we tested the hypothesis that tumor necrosis factor (TNF)- , interferon (IFN)- , and LPS can increase DMT1 expression in airway epithelial cells. We used RT-PCR to detect mRNA for both -IRE DMT1 and +IRE DMT1 in BEAS-2B cells. Treatment with TNF-, IFN- , or LPS increased both forms. Western blot analysis also demonstrated an increase in the expression of both isoforms of DMT1 increased after these treatments. Twenty-four hours after exposure of an animal model to TNF- , IFN- , or LPS, a significant increase in pulmonary expression of -IRE DMT1 was seen by immunohistochemistry; the level of +IRE DMT1 was too low in the lung to be visualized using this methodology. Finally, iron transport into BEAS-2B cells was increased after inclusion of TNF- , IFN- , or LPS in the media. We conclude that pro-inflammatory cytokines and LPS increase mRNA and protein expression of DMT1 in airway cells. Both -IRE and +IRE isoforms are elevated after exposures. Increased expression of this protein appears to be included in a coordinated response of the cell and tissue where the function might be to diminish availability of metal. During inflammation, respiratory epithelial cells participate in the development of hypoferremia comparable to monocytic cells.