Mechanisms of fibronectin-binding protein A (FnBPA110–263) vaccine efficacy in Staphylococcus aureus sepsis versus skin infection

Publication date: September 2018

Source: Clinical Immunology, Volume 194

Author(s): Rui Zhang, Sun Li, Xiao-Kai Zhang, Yu Wang, Liu-Yang Yang, Hao Zeng, Da-Peng Yan, Quan-Ming Zou, Qian-Fei Zuo

Abstract

Increasing rates of life-threatening infections and decreasing susceptibility to antibiotics urge an effective vaccine targeting Staphylococcus aureus. Here we investigate the role of cellular immunity in FnBPA_110–263 mediated protection in Staphylococcus aureus infection. This study revealed FnBPA_110–263 broadly protected mice from seven FnBPA isotypes strains in the sepsis model. FnBPA_110–263 immunized B-cell deficient mice were protected against lethal challenge, while T-cell deficient mice were not. Reconstituting mice with FnBPA_110–263 specific CD4+ T-cells conferred antigen specific protection. In vitro assays indicated that isolated FnBPA_110–263 specific splenocytes from immunized mice produced abundant IL-17A. IL-17A deficient mice were not protected from a lethal challenge by FnBPA_110–263 vaccination. Moreover, neutralizing IL-17A, but not IFN-γ,reverses FnBPA_110–263-induced protective efficacy in sepsis and skin infection model. These findings suggest that IL-17A producing Th17 cells play an essential role in FnBPA_110–263 vaccine-mediated defense against S. aureus sepsis and skin infection in mice.

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