Comparison of the host responses to wild-type and cpsB mutant Klebsiella pneumoniae infections

Previously, we established an intranasal mouse model of Klebsiella pneumoniae infection and validated its utility using a highly virulent wild-type strain and an avirulent capsular polysaccharide mutant. In the present study we compare the host responses to both infections by examining cytokine production, cellular infiltration, pulmonary histology, and intranasal immunization. Klebsiella pneumoniae has been known as an important cause of gram-negative bacterial pneumonia for more than 100 years. The best-characterized virulence factor of this species is capsular polysaccharide, a voluminous layer of acidic sugar polymers responsible for a variety of K. pneumoniae pheno-types, including protection against complement-mediated kill-ing and inhibition of macrophage phagocytosis (6, 11). Capsule has also been investigated using a number of different animal models for its importance in K. pneumoniae pathogenesis. Iso-genic capsule mutant strains are deficient for causing disease in mice via intraurethral and intratracheal inoculation route