IL-17A secreted by Th17 cells is essential for the host against Streptococcus agalactiae infections.

Streptococcus agalactiae is an important bacterial pathogen that is the causative agent of diseases, including neonatal sepsis and meningitis, and infections in pregnant women and non-pregnant adults. Although antibiotic treatments effectively relieve symptoms, the emergence and transmission of multidrug-resistant strains indicate the need for an effective immunotherapy. Effector T helper (Th) 17 cells is a relatively newly discovered subpopulation of helper CD4+ T lymphocytes, by expressing interleukin (IL)-17A play crucial roles in host defenses against a variety of pathogens, including bacteria and viruses. However, whether S. agalactiae infection can induce the differentiation of CD4+ T cells into Th17 cells, and whether IL-17A can play an effective role against S. agalactiae infections, are still unclear. In this study, we analyzed the responses of CD4+ T cells and their defensive effects after S. agalactiae infection. The results showed that S. agalactiae infection induce not only the formation of Th1 cells expressing interferon (IFN)-γ, but also the differentiation of mouse splenic CD4+ T cells into Th17 cells, which highly express IL-17A. In addition, the bacterial load of S. agalactiae was significantly increased and decreased in organs as determined by antibody neutralization and IL-17A addition experiments, respectively. The results confirmed that IL-17A is required by the host to defend against S. agalactiae and that it plays an important role in effectively eliminating S. agalactiae. The results prompt us to adopt effective methods to regulate the expression of IL-17A as an effective strategy for the prevention from and treatment of S. agalactiae infection.