By contrast, the recovery phase is marked by persistent infiltration of neutrophils and monocytes, increased TLR4 and angiogenesis, failure to engage pro-resolving programs due to loss of eosinophils and CD206+/Tim4+ macrophages, downregulation of type I interferon and metabolic pathways, and limited restoration of gut microbiota following CDI. Here, TIMD4 is linked to clostridium difficile infection.