The integration of knowledge concerning the regulation of metallothionein (MT) with research on its proposed
functions is necessary to clarify how MT affects cellular processes. MT expression is induced/enhanced in various tissues
by a number of physiological mediators through several response elements in the MT gene promoter. The cellular accumulation
of MT depends on the availability of cellular zinc derived from the diet. MT modulates: 1) the binding and exchange/
transport of heavy metals such as zinc, cadmium, or copper under physiological conditions and cytoprotection
from their toxicities, and 2) the release of gaseous mediators such as hydroxyl radicals or nitric oxide. In addition, MT reportedly
affects a number of cellular processes, such as gene expression, apoptosis, proliferation, and differentiation.
Given the genetic approach, the apparently healthy status of MT-deficient mice argues against an essential biological role
for MT; however, the molecule may be critical in cells/tissues/organs in times of stress, since MT expression is also
evoked/enhanced by various stresses. In particular, because metallothionein (MT) is induced by inflammatory stress, its
roles in inflammation are implied. Also, MT expression in the lung can be enhanced by inflammatory stimuli, suggesting
that its expression correlates with inflammatory pulmonary diseases. In this paper, we review the role of MT of various inflammatory
conditions in the airway.