While the main responding immune cell to infection with C. difficile is thought to be neutrophils, eosinophils and innate lymphoid cells have also been shown to play an important role in host protection from disease. These cells produce IL-4 and IL-13, two closely related cytokines that often have important roles in type 2 immunity. Neutralization of either of these cytokines leads to a delayed recovery of the host from disease, while administration hastened recovery, suggesting that these cytokines may promote responses that are important for this phase. I aim to characterize the roles of these cytokines to determine how they contribute to host protection and recovery, and what downstream factors may be carrying out effector functions. As certain macrophages expressing IL-4Ra (the receptor important for both cytokines’ signaling) increase throughout infection, I also aim to determine whether IL-4 and IL-13 promote the polarization and expansion of alternatively-activated macrophages (AAMs), and whether these cells are a player in promoting host recovery.