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2016 ; 11
(5
): e0156298
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Autophagy Induced by Intracellular Infection of Propionibacterium acnes
#MMPMID27219015
Nakamura T
; Furukawa A
; Uchida K
; Ogawa T
; Tamura T
; Sakonishi D
; Wada Y
; Suzuki Y
; Ishige Y
; Minami J
; Akashi T
; Eishi Y
PLoS One
2016[]; 11
(5
): e0156298
PMID27219015
show ga
BACKGROUND: Sarcoidosis is caused by Th1-type immune responses to unknown agents,
and is linked to the infectious agent Propionibacterium acnes. Many strains of P.
acnes isolated from sarcoid lesions cause intracellular infection and autophagy
may contribute to the pathogenesis of sarcoidosis. We examined whether P. acnes
induces autophagy. METHODS: Three cell lines from macrophages (Raw264.7),
mesenchymal cells (MEF), and epithelial cells (HeLa) were infected by viable or
heat-killed P. acnes (clinical isolate from sarcoid lymph node) at a multiplicity
of infection (MOI) of 100 or 1000 for 1 h. Extracellular bacteria were killed by
washing and culturing infected cells with antibiotics. Samples were examined by
colony assay, electron-microscopy, and fluorescence-microscopy with anti-LC3 and
anti-LAMP1 antibodies. Autophagy-deficient (Atg5-/-) MEF cells were also used.
RESULTS: Small and large (?5 ?m in diameter) LC3-positive vacuoles containing few
or many P. acnes cells (LC3-positive P. acnes) were frequently found in the three
cell lines when infected by viable P. acnes at MOI 1000. LC3-positive large
vacuoles were mostly LAMP1-positive. A few small LC3-positive/LAMP1-negative
vacuoles were consistently observed in some infected cells for 24 h
postinfection. The number of LC3-positive P. acnes was decreased at MOI 100 and
completely abolished when heat-killed P. acnes was used. LC3-positive P. acnes
was not found in autophagy-deficient Atg5-/- cells where the rate of infection
was 25.3 and 17.6 times greater than that in wild-type Atg5+/+ cells at 48 h
postinfection at MOI 100 and 1000, respectively. Electron-microscopic examination
revealed bacterial cells surrounded mostly by a single-membrane including the
large vacuoles and sometimes a double or multi-layered membrane, with occasional
undigested bacterial cells in ruptured late endosomes or in the cytoplasm.
CONCLUSION: Autophagy was induced by intracellular P. acnes infection and
contributed to intracellular bacterial killing as an additional host defense
mechanism to endocytosis or phagocytosis.
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