Mapping the pulmonary environment of animals protected from virulent H1N1 influenza infection using the TLR‐2 agonist Pam 2 Cys

We have previously shown that intranasal administration of the Toll‐like receptor‐2 agonist, S‐(2,3‐bis(palmitoyloxy)propyl) cysteine (Pam 2 Cys), provides immediate and antigen independent protection against challenge with influenza virus. Here we characterize the cellular pulmonary environments of mice which had either been treated with Pam 2 Cys or placebo and then challenged with influenza virus. We show that Pam 2 Cys treatment results in the influx of innate immune cells into the lungs and that depletion of phagocytic cells from this influx using clodronate‐loaded liposomes caused a reduction in the number of interstitial macrophages and monocytes. This resulted in abolition of the protective effect indicating the importance of this cellular subset in Pam 2 Cys‐mediated protection.