The termination of the inflammatory process was supported by a marked decrease in IL-6, TNF-α, and NF-κB, which are known to enhance inflammation in early ALI (Suratt and Parsons 2006; Devaney et al. 2013) and increase anti-inflammatory cytokines IL-10, which was found to reduce neutrophilic activity and inflammatory mediators in ALI in LPS mice model (Inoue 2000) compared to PC group. The gene discussed is NFKB1; the disease is acute respiratory distress syndrome.