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Pf Bacteriophage and Their Impact on Pseudomonas Virulence, Mammalian Immunity, and Chronic Infections

Abstract

Pf bacteriophage are temperate phages that infect the bacterium , a major cause of chronic lung infections in cystic fibrosis (CF) and other settings. Pf and other temperate phages have evolved complex, mutualistic relationships with their bacterial hosts that impact both bacterial phenotypes and chronic infection. We and others have reported that Pf phages are a virulence factor that promote the pathogenesis of infections in animal models and are associated with worse skin and lung infections in humans. Here we review the biology of Pf phage and what is known about its contributions to pathogenesis and clinical disease. First, we review the structure, genetics, and epidemiology of Pf phage. Next, we address the diverse and surprising ways that Pf phages contribute to phenotypes including effects on biofilm formation, antibiotic resistance, and motility. Then, we cover data indicating that Pf phages suppress mammalian immunity at sites of bacterial infection. Finally, we discuss recent literature implicating Pf in chronic infections in CF and other settings. Together, these reports suggest that Pf bacteriophage have direct effects on infections and that temperate phages are an exciting frontier in microbiology, immunology, and human health.

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References
1.
Ciofu O, Bagge N, Hoiby N . Antibodies against beta-lactamase can improve ceftazidime treatment of lung infection with beta-lactam-resistant Pseudomonas aeruginosa in a rat model of chronic lung infection. APMIS. 2003; 110(12):881-91. DOI: 10.1034/j.1600-0463.2002.1101207.x. View

2.
Miernikiewicz P, Dabrowska K, Piotrowicz A, Owczarek B, Wojas-Turek J, Kicielinska J . T4 phage and its head surface proteins do not stimulate inflammatory mediator production. PLoS One. 2013; 8(8):e71036. PMC: 3745418. DOI: 10.1371/journal.pone.0071036. View

3.
Bjarnsholt T . The role of bacterial biofilms in chronic infections. APMIS Suppl. 2013; (136):1-51. DOI: 10.1111/apm.12099. View

4.
Bonfield T, Panuska J, Konstan M, Hilliard K, Hilliard J, Ghnaim H . Inflammatory cytokines in cystic fibrosis lungs. Am J Respir Crit Care Med. 1995; 152(6 Pt 1):2111-8. DOI: 10.1164/ajrccm.152.6.8520783. View

5.
Rao S, Coleman P . Control of DNA replication and cell growth by inhibiting the export of mitochondrially derived citrate. Exp Cell Res. 1989; 180(2):341-52. DOI: 10.1016/0014-4827(89)90062-1. View