While the pattern of production and the role of IL-1α appeared to mirror that of IL-1β, IL-18 showed a bimodal peak production, being expressed both in the early and the late phases of the infection; moreover, neutralization of IL-18 resulted in worsened vaginal pathology and increased levels of myeloperoxidase, S100A8 and S100A9 (8). Here, IL1A is linked to infection.