The involvement of IL-1 was confirmed by infection of Il-1β−/− mice and the phenotype of the Il-1β−/− mice was quite convincing, as the difference in bacterial persistence between CFT073 and the TcpC deficient mutant in wt mice was abrogated in Il-1β−/− mice and the innate immune response to the two isogenic strains was similar. The gene discussed is IL1A; the disease is infection.