This conclusion is supported by: 1) the early incidence of elevations in S100A8 and S100A9 expression along with resident neutrophil influx, 2) the fact that the mice were maintained in sterile environments without detectable lung pathogens, and 3) elevated S100A8 levels were detected in the B6-CF lungs but not Bc-CF airways maintained in identical environments. Here, S100A9 is linked to cystic fibrosis.