While TLR4 was necessary to initiate airway inflammation shown by reduced neutrophil, lymphocyte, and eosinophilia recruitment as well as IL-4 and IL-10 cytokines in the lungs in TLR4-KO or -antagonized mice immunized with BPE, compared to mice treated with PBS, the downstream adaptor TRIF had the contrary effect of dampening the inflammatory response induced by BPE airway exposure. Here, TLR4 is linked to Increased total eosinophil count.