TitleThe ability to form biofilm influences Mycobacterium avium invasion and translocation of bronchial epithelial cells.
Publication TypeJournal Article
Year of Publication2006
AuthorsYamazaki, Y, Danelishvili, L, Wu, M, Hidaka, E, Katsuyama, T, Stang, B, Petrofsky, M, Bildfell, R, Bermudez, LE
JournalCell Microbiol
Date Published2006 May
KeywordsAnimals, Bacterial Adhesion, Biofilms, Bronchi, Cell Line, DNA Transposable Elements, Epithelial Cells, Humans, Integrin beta1, Mice, Microscopy, Electron, Mutation, Mycobacterium avium Complex, Mycobacterium avium-intracellulare Infection, Respiratory Mucosa

Organisms of the Mycobacterium avium complex (MAC) are widely distributed in the environment, form biofilms in water pipes and potable water tanks, and cause chronic lung infections in patients with chronic obstructive pulmonary disease and cystic fibrosis. Pathological studies in patients with pulmonary MAC infection revealed granulomatous inflammation around bronchi and bronchioles. BEAS-2B human bronchial epithelial cell line was used to study MAC invasion. MAC strain A5 entered polarized BEAS-2B cells with an efficiency of 0.1 +/- 0.03% in 2 h and 11.3 +/- 4.0% in 24 h. In contrast, biofilm-deficient transposon mutants 5G4, 6H9 and 9B5 showed impaired invasion. Bacteria exposed to BEAS-2B cells for 24 h had greater ability to invade BEAS-2B cells compared with bacteria incubated in broth. M. avium had no impact on the monolayer transmembrane resistance. Scanning electron microscopy showed that MAC A5 forms aggregates on the surface of BEAS-2B cell monolayers, and transmission electron microscopy evidenced MAC within vacuoles in BEAS-2B cells. Cells infected with the 5G4 mutant, however, showed significantly fewer bacteria and no aggregates on the cell surface. Mutants had impaired ability to cause infection in mice, as well. The ability to form biofilm appeared to be associated with the invasiveness of MAC A5.

Alternate JournalCell Microbiol
PubMed ID16611229
Grant ListAI-43199 / AI / NIAID NIH HHS / United States