Over time, both the types of bacteria and their individual characteristics change in individuals with CF. In the initial stage, common bacteria such as "S. aureus" and "H. influenzae" colonize and infect the lungs. Eventually, "Pseudomonas aeruginosa" (and sometimes "Burkholderia cepacia") dominates. By 18 years of age, 80% of patients with classic CF harbor "P. aeruginosa", and 3.5% harbor "B. cepacia". Once within the lungs, these bacteria adapt to the environment and develop resistance to commonly used antibiotics. "Pseudomonas" can develop special characteristics that allow the formation of large colonies, known as "mucoid" "Pseudomonas", which are rarely seen in people who do not have CF. Scientific evidence suggests the interleukin 17 pathway plays a key role in resistance and modulation of the inflammatory response during "P. aeruginosa" infection in CF. In particular, interleukin 17-mediated immunity plays a double-edged activity during chronic airways infection; on one side, it contributes to the control of "P. aeruginosa" burden, while on the other, it propagates exacerbated pulmonary neutrophilia and tissue remodeling.