The ability to form biofilm influences Mycobacterium avium invasion and translocation of bronchial epithelial cells

被引:91
作者
Yamazaki, Y
Danelishvili, L
Wu, M
Hidaka, E
Katsuyama, T
Stang, B
Petrofsky, M
Bildfell, R
Bermudez, LE [1 ]
机构
[1] Oregon State Univ, Coll Vet Med, Dept Biomed Sci, Corvallis, OR 97331 USA
[2] Oregon State Univ, Coll Sci, Dept Microbiol, Corvallis, OR 97331 USA
[3] Sinshu Univ, Sch Med, Dept Lab Med, Matsumoto, Nagano 3908621, Japan
[4] Calif Pacific Med Ctr, Res Inst, Kuzell Inst, San Francisco, CA USA
关键词
D O I
10.1111/j.1462-5822.2005.00667.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:806 / 814
页数:9
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