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Pseudomonas aeruginosa induces localized immunosuppression during pneumonia
被引:77
作者:
Diaz, Maureen H.
[1
]
Shaver, Ciara M.
[1
]
King, John D.
[1
]
Musunuri, Srinidhi
[2
]
Kazzaz, Jeffrey A.
[3
,4
,5
]
Hauser, Alan R.
[1
,6
]
机构:
[1] Northwestern Univ, Dept Immunol Microbiol, Chicago, IL 60611 USA
[2] Northwestern Univ, Dept Pathol, Chicago, IL 60611 USA
[3] Winthrop Univ Hosp, CardioPulm Res Inst, Mineola, NY 11501 USA
[4] Winthrop Univ Hosp, Div Pulm & Crit Care Med, Mineola, NY 11501 USA
[5] SUNY Stony Brook, Mineola, NY USA
[6] Northwestern Univ, Dept Med, Chicago, IL 60611 USA
关键词:
D O I:
10.1128/IAI.00012-08
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Hospital-acquired bacterial pneumonia is a common and serious complication of modern medical care. Many aspects of such infections remain unclear, including the mechanisms by which invading pathogens resist clearance by the innate immune response and the tendency of the infections to be polymicrobial. Here, we used a mouse model of infection to show that Pseudomonas aeruginosa, a leading cause of hospital-acquired pneumonia, interferes with the ability of recruited phagocytic cells to eradicate bacteria from the lung. Early in infection, phagocytic cells, predominantly neutrophils, are recruited to the lungs but are incapacitated when they enter the airways by the P. aeruginosa toxin ExoU. The resulting paucity of functioning phagocytes allows P. aeruginosa to persist within the lungs and results in local immunosuppression that facilitates superinfection with less-pathogenic bacteria. Together, our results provide explanations for previous reports linking ExoU-secreting P. aeruginosa with more severe pulmonary infections and for the tendency of hospital-acquired pneumonia to be polymicrobial.
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页码:4414 / 4421
页数:8
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