In the acute phase, at 3-weeks post-infection (WPI), the Δami1 mutant significantly increased the production of several proinflammatory cytokines (IFN-γ and TNF), type 1 interferon (IFN-β), regulatory cytokines (TGFβ and IL-10), and chemokines (CCL2, CCL3, CXCL1, CXCL5, and CXCL10) in whole lung homogenates when compared to the Δami1 complemented and wild-type strains (Figure 3(a)). The gene discussed is CCL3; the disease is infection.