期刊
JOURNAL OF CELL SCIENCE
卷 125, 期 2, 页码 507-515出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.094573
关键词
Extracellular bacteria; Punctation; Autophagolysosome; Host defense; Respiratory immunity
类别
资金
- National Institutes of Health [5R03 ES014690, 5R01HL092905-04, 3R01HL092905-02S1]
- National 973 Basic Research Program of China [2012CB518900]
- American Heart Association [535010N]
Intracellular bacteria have been shown to cause autophagy, which impacts infectious outcomes, whereas extracellular bacteria have not been reported to activate autophagy. Here, we demonstrate that Pseudontonas aeruginosa, a Gram-negative extracellular bacterium, activates autophagy with considerably increased LC3 punctation in both an alveolar macrophage cell line (MH-S) and primary alveolar macrophages. Using the LC3 Gly120 mutant, we successfully demonstrated a hallmark of autophagy, conjugation of LC3 to phosphatidylethanolamine (PE). The accumulation of typical autophagosomes with double membranes was identified morphologically by transmission electron microscopy (TEM). Furthermore, the increase of PE-conjugated LC3 was indeed induced by infection rather than inhibition of lysosome degradation. P. aeruginosa induced autophagy through the classical beclin-1-Atg7-Atg5 pathway as determined by specific siRNA analysis. Rapamycin and IFN-gamma (autophagy inducers) augmented bacterial clearance, whereas beclin-1 and Atg5 knockdown reduced intracellular bacteria. Thus, P. aeruginosa-induced autophagy represents a host protective mechanism, providing new insight into the pathogenesis of this infection.
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