Mucin is a glycoprotein that is the primary component of the mucus overlaying 
the epithelial tissues. Because mucin functions as a first line of the innate 
immune system, Pseudomonas aeruginosa appears to require interaction with mucin 
to establish infection in the host. However, the interactions between P. 
aeruginosa and mucin have been poorly understood. In this study, using in vivo 
expression technology (IVET), we attempted to identify mucin-inducible promoters 
that are likely to be involved in the establishment of P. aeruginosa infection. 
The IVET analysis revealed that the genes encoding glycosidases, sulfatases, and 
peptidases that are thought to be required for the utilization of mucin as a 
nutrient are present in 13 genes downstream of the identified promoters. Our 
results indicated that, among them, sdsA1 encoding a secreted sulfatase plays a 
central role in the degradation of mucin. It was then demonstrated that 
disruption of sdsA1 leads to a decreased release of sulfate from mucin and 
sulfated sugars. Furthermore, the sdsA1 mutant showed a reduction in the ability 
of mucin gel penetration and an attenuation of virulence in leukopenic mice 
compared with the wild-type strain. Collectively, these results suggest that 
SdsA1 plays an important role as a virulence factor of P. aeruginosa.