Open AccessThe ability to form biofilm influences Mycobacterium avium invasion and translocation of bronchial epithelial cells
Author(s) -
Yamazaki Yoshitaka,
Danelishvili Lia,
Wu Martin,
Hidaka Eiko,
Katsuyama Tsutomu,
Stang Bernadette,
Petrofsky Mary,
Bildfell Robert,
Bermudez Luiz E.
Publication year - 2006
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2005.00667.x
Subject(s) - microbiology and biotechnology , biology , biofilm , vacuole , bacteria , mutant , cytoplasm , biochemistry , genetics , gene
Summary 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.