The authors would like to give appreciation to Brian Belt, Stacy Suess, and Jesse Gibbs for their technical support and assistance in experiments.
Disclosures The authors have no financial conflict of interest. 3Abbreviations used in this paper: DC, dendritic cell; ��-GC, ��-galactosylceramide; ASGM1, asialo GM1; cIg, control Ig; WT, wild type; GEM, gemcitabine; Dox, doxorubicin; http://www.selleckchem.com/products/Erlotinib-Hydrochloride.html 5-FU-, 5-fluoracil; Treg, regulatory T cell; DLN, draining lymph node. 1M.J.S. was supported by a National Health and Medical Research Council of Australia Senior Principal Research Fellowship and a Cancer Council of Victoria Project Grant. M.W.L.T. was supported by a National Health and Medical Research Council Doherty Fellowship and the Cancer Council of Victoria. M.A.E. was supported by National Institutes of Health Grant DK66917.

www.jimmunol.org/cgi/doi/10.4049/jimmunol.0900796
In cystic fibrosis (CF) patients, chronic Pseudomonas aeruginosa infection and inflammation are associated with biofilm formation, a progressive decline in lung function and premature death [1], [2], [3]. Early infection of CF infants with P. aeruginosa is usually successfully managed by aggressive antibiotic therapy; however by adolescence most patients have chronic infection. Prominent persisters include the frequent clones Liverpool Epidemic Strain (LES), Manchester strain (c3719), and the Australian Epidemic Strain-1 (AES-1), which infects ca. 40% of adult CF patients in Sydney and Melbourne [4], [5]. While frequent clones are often more resistant to antibiotics than infrequent clones, they lack a distinctive antibiotic resistance profile [6], indicating that other factors are involved in their persistence.

P. aeruginosa undergo a number of genetic and expression changes that assist in their ability to survive in the CF lung and to evade detection and clearance by the immune system [7], [8]. Acute lung infection in CF patients is associated with expression of virulence determinants that are involved in establishment of infection in animal model systems [9], [10], [11], [12]. However, P. aeruginosa from chronically-infected CF patients usually lack some of these virulence determinants, suggesting that these genes are unnecessary for long-term maintenance of P. aeruginosa infection in vivo [13], [14], [15]. Genomic studies of two closely related P. aeruginosa strains collected from a CF patient 7.

5 years apart [14] showed loss of function mutations in virulence genes required for O-antigen biosynthesis, Type III secretion (T3SS), twitching motility, exotoxin A regulation, Brefeldin_A multidrug efflux, osmotic balance, phenazine biosynthesis, quorum sensing, and iron acquisition. Chronic infection strains also possess particular characteristics, including large chromosomal inversions (LCI) [16], a specific Type IV pilin allele [17], exhibit enhanced biofilm dispersal properties [18] and a progressive loss of T3SS function over time [19].