Abstract
Abstract The IL-17 family of cytokines phylogenetically pre-dates the evolution of T-cells in jawed vertebrates, suggesting that the ontogeny of the Th17 lineage must have arisen to confer an evolutionary advantage to the host over innate sources of IL-17. Using a model of mucosal immunization with the encapsulated bacteria, Klebsiella pneumoniae, we show that intranasal immunization strongly induces IL-17 producing cells in the lung. Further analysis reveals that these cells are conventional Th17 cells and are antigen specific as they proliferate and produce IL-17 upon re-stimulation with heat-killed K. pneumoniae but not heat-killed Escherichia coli or Staphylococcus aureus. In vivo, immunization induced Th17 cells but not Th1 cells undergo activation/expansion and contraction overtime and the Th17 responses together with anit-K. pneumoniae antibody responses lead to the protection of immunized mice from live K. pneumoniae infection. However, B-cell/antibody mediated protection is limited only to the vaccine strain. In contrast memory Th17 cells proliferate in response to conserved outer membrane proteins and confer protection against subsequent bacterial challenge with several serotypes of K. pneumoniae, including the recently described multi-drug resistant New Delhi metallolactamase strain. These data suggest that Th17 adjuvants can improve vaccination strategies against drug resistant encapsulated bacteria.
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