Pulmonary and systemic inflammation plays a key role in the prognosis of patients with acute lung injury ALI. Lipopolysaccharide (LPS)-induced ALI is a classical model to study new treatments for ALI. Here, Escherichia coli LPS (026:B6; L3755, Sigma Aldrich, St. Louis, MO, USA) were administered intra-peritoneally (i.p.) in male C57Bl/6 mice to induce ALI. Control (n=12), Virlaza (50ul intra-nasally; n=12), LPS (100ug i.p.; n=12) and LPS+Virlaza (100ug i.p. +50ul intra-nasally; n=12) were studied. The results demonstrated that Virlaza reduced the number of total leukocytes (p<0.01), neutrophils (p<0.01), lymphocytes (p<0.01) and macrophages (p<0.01) in the bronchoalveolar lavage (BAL), while also reduced the BAL levels of IL-1beta (p<0.01), IL-6 (<0.01), CXCL1/KC (p<0.01), IL-17 (p<0.01) and TNF-alpha (p<0.01). Virlaza increased the levels of anti-inflammatory cytokine IL-10 (p<0.001). Virlaza reduced the accumulation of neutrophils (p<0.05), lymphocytes (p<0.05) and macrophages (p<0.05) in the lung parenchyma. In addition, Virlaza also inhibited LPS-induced systemic inflammation, as denoted by reduced number of total leukocytes (p<0.01), neutrophils (p<0.001), lymphocytes (p<0.05), and monocytes (p<0.01). Of note, Virlaza also reduced the serum levels of IL-1beta (p<0.05), IL-6 (<0.001), CXCL1/KC (p<0.05), IL-17 (p<0.001) and TNF-alpha (p<0.001), while increased the levels of IL-10 (p<0.001). Thus, we conclude that Virlaza possesses potent pulmonary and systemic anti-inflammatory effects against bacterial infection, which deserves further clinical trials to confirm such pre-clinical findings.