We compared the production of cytokines, chemokines and PGE2 in response to either TLR3, TLR2, or TLR2/6 agonists alone, with the response to TLR2 or TLR2/6 agonists following TLR3 priming in PBMCs as a model of systemic infection and inflammation, and in placental explants as a model of haematogenous spread of multi-pathogen infection. Here, TLR2 is linked to infection.