Although TLR2 was previously found to be required for protection from increased bacterial burden in a sepsis model of S. aureus infection (55), we found that the presence/absence of TLR2, in the absence of virus/capsid inoculation, does not affect the bacterial burden in our pneumonia model, suggesting the observed responses are due to the initial antiviral response in the lung environment. This evidence concerns the gene TLR2 and susceptibility to pneumonia measurement.