The administration of antibiotics causes the dysbiosis of commensal microbial populations, which can lead to colonization by vancomycin-resistant Enterococcus faecium (VRE) and, potentially, sepsis in compromised patients. In Science Translational Medicine, Pamer and colleagues show that triggering antiviral innate immunity restores resistance to VRE. The receptor TLR7 normally recognizes viral RNA but can be stimulated with the synthetic ligand resiquimod (R-848). Oral administration of R-848 stimulates CD11c+ dendritic cells to induce expression of IL-23. In turn, IL-23 triggers IL-22 expression in gut innate lymphoid cells, which leads to the expression of antimicrobial peptides, including Reg3g. This innate immune response helps to diminish VRE numbers in the gut after antibiotic-induced dysbiosis, which suggests a means for helping to control enterococcal infections in vunerable patients.

Sci. Transl. Med. 8, 327ra25 (2016)