AIRmax and AIRmin
mouse lines show a differential
lung inflammatory response and differential
lung tumor susceptibility after
urethane treatment. The transcript profile of 24,000 known
genes was analyzed in normal
lung tissue of untreated and
urethane-treatedAIRmax and AIRmin
mice. In
lungs of untreated
mice,
inflammation-associated
genes involved in pathways such as
leukocyte transendothelial migration,
cell adhesion and
tight junctions were differentially expressed. Moreover,
gene expression levels differed significantly in
urethane-treated
mice; in AIRmin
mice, modulation of expression of
genes involved in pathways associated with inflammatory response paralleled the previously observed persistent infiltration of inflammatory
cells in the
lung of these
mice.