Therefore, mice double deficient in IL-1α plus IL-1β develop a rapid, exacerbated lung inflammation which may be the result of uncontrolled bacterial infection, as seen in IL-1R1 or TNF deficient mice, but expression of either IL-1α or IL-1β was sufficient to contribute to the host control of bacterial growth and lung inflammation during acute M. tuberculosis infection. The gene discussed is IL1A; the disease is inflammatory response.