Given the reported crucial importance of MYD88 for the inflammatory response, the observed downregulation of MYD88 in the PCLS model could be another mechanism the host employs to hinder an exacerbated inflammatory response during 8067 and T15 infection, contributing to the observed lowered/lack of virulence of these strains in vivo compared to S10. The gene discussed is MYD88; the disease is infection.