In accordance with data that TH1 as well as IL-17A and IL-22 are drastically increased in several lung and other infection models [11,33,34], we first showed that bacterial challenge with P. aeruginosa of lungs in non-ventilated rats induced a significant increase in TH17 cytokines (IL-17A, IL-17F, and IL-22) and TH1 cytokines (IFNγ, TNFα, IL-6, and IL-1β) compared to the non-infected/non-ventilated control group. The gene discussed is IL17A; the disease is infection.