We also want to introduce another candidate for an indicator of active pulmonary tuberculosis. Metallothionein is a highly conserved, low-molecular-weight, cysteine-rich protein. Metallothionein has been proposed to play an important role in homeostasis and detoxication of heavy metals. Metallothionein can serve as a sacrificial scavenger for hydroxyl radicals in vitro2and protects against free radical-induced DNA damage.3–5 Since proinflammatory cytokines, including tumor necrosis factor-α, interleukin (IL)-1, IL-6, and interferon-γ, induce hepatic metallothionein gene expression, the role of metallothionein in inflammatory diseases has been focused. Recently, we have demonstrated that metallothionein-null (-/-) mice were more susceptible than corresponding wild-type mice to lung inflammation, especially to lung edema, which were induced by intratracheal challenge with bacterial endotoxin.6 We confirmed that metallothionein proteins in the lungs were detected in endothelial cells and alveolar epithelial cells of wild-type mice, whereas they were not detected in those of metallothionein (-/-) mice by immunohistochemistry. After endotoxin challenge, metallothionein deficiency enhanced vacuolar degeneration of pulmonary endothelial cells and type I alveolar epithelial cells, and caused focal loss of the basement membrane without any significant differences in the enhanced local (lung) expression of proinflammatory cytokines and chemokines or in the activation of nuclear factor-κB pathway in the lung between the two genotypes. We concluded that endogenous metallothionein is defensive against acute lung injury related to bacterial endotoxin, possibly via the protection of pulmonary vascular integrity.6 Additional researches targeting metallothionein in pulmonary tuberculosis might throw new therapeutic strategies to this persistent infectious disease.