The risk of Pseudomonas aeruginosa (Pa) acquisition, colonization, and infection during chronic bronchial disease varies according to the disease (cystic fibrosis, bronchial dilatation, post-tobacco abuse chronic obstructive bronchopneumonia), its evolutive stage, and a number of known or suspected factors. The involvement of Pa marks an important evolution of the disease, well demonstrated in cystic fibrosis. P. aeruginosa can adhere to epithelial cells (initial colonization) then organizes itself in complex structures evolving from simples microcolonies to macrocolonies in a structured biofilm supporting chronic colonization. P. aeruginosa can produce several factors of virulence, leading to the permanent destruction of host cells, thus inducing the regular liberation of pro-inflammatory mediators implementing a vicious circle worsening these chronic respiratory diseases and favoring their exacerbation. Chronic Pa suppuration has a systemic impact and justifies a global multidisciplinary management. In cystic fibrosis, the presence of P. aeruginosa is a major prognostic element. The current consensus is to detect the primary colonization as early as possible eradication is still possible and to treat it before it evolves to chronicity. But right now, this type of management has not been justified for other chronic bronchial diseases.