Finally, since both the B6-CF and Bc-CF mice were maintained in identical environments, the differential levels of S100A8 expression between the two strains is likely influenced by secondary genetic factors acting on neutrophils (either intrinsically or through the pulmonary interstitial milieu) to either suppress or upregulate its expression in the Bc or B6 strain, respectively, rather than the effect of differential environmental exposures or infection status. Here, S100A8 is linked to infection.