title: Impact of multidrug resistance on experimental empyema by Pseudomonas aeruginosa.
abstract: BACKGROUND
  Pseudomonas aeruginosa is a cause of infections of the lower respiratory tract among patients with chronic lung disorders. It is questionable whether virulence of this species may be influenced by multidrug resistance (MDR).
  
  
  OBJECTIVE
  To define the impact of MDR in experimental lung infection.
  
  
  METHODS
  Experimental empyema was induced in rabbits by MDR (group A, n = 16) and by susceptible isolates (group B, n = 10). Pleural fluid was sampled for quantitative culture and estimation of cell apoptosis and of tumor necrosis factor-alpha (TNFα) and malondialdehyde (MDA). Survival was recorded. Cytokine production was stimulated in U937 monocytes by samples of pleural fluid. Whole blood of rabbits was incubated with the isolates; induction of apoptosis was assessed.
  
  
  RESULTS
  Survival of group A was prolonged compared to group B. This was accompanied by lower bacterial counts of the inoculated pathogens in pleural fluid and in the lungs of group A compared with group B. Early apoptosis of neutrophils of pleural fluid of group A was lower compared with group B. Pleural fluid concentrations of TNFα and MDA did not differ between the groups. Cytokine production by U937 monocytes after stimulation with pleural fluid was greater in group B than in group A. The susceptible isolate induced apoptosis of neutrophils in vitro at a greater rate than the MDR isolate.
  
  
  CONCLUSIONS
  Experimental empyema by susceptible P. aeruginosa is accompanied by greater mortality compared with MDR P. aeruginosa. This phenomenon may be attributed to the different growth pattern of the pathogens or to their interaction with the innate immune system.
authors.affiliation: 4th Department of Internal Medicine, University of Athens, Medical School, Athens, Greece. giamarel @ ath.forthnet.gr
authors.forename: Evangelos J
authors.initials: EJ
authors.lastname: Giamarellos-Bourboulis
authors.forename: Ira
authors.initials: I
authors.lastname: Tzepi
authors.forename: Irini
authors.initials: I
authors.lastname: Tsovolou
authors.forename: Aikaterini
authors.initials: A
authors.lastname: Spyridaki
authors.forename: Thomas
authors.initials: T
authors.lastname: Tsaganos
authors.forename: Ilia
authors.initials: I
authors.lastname: Vaki
authors.forename: Antigone
authors.initials: A
authors.lastname: Kotsaki
authors.forename: Vlasios
authors.initials: V
authors.lastname: Polychronopoulos
mesh_terms: D000818:Animals; D058491:Bacterial Load; D016207:Cytokines / Q000096:biosynthesis; D004198:Disease Susceptibility; D024901:Drug Resistance, Multiple, Bacterial / Q000502:physiology; D004653:Empyema / Q000382:microbiology* / Q000401:mortality; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology; D008168:Lung / Q000382:microbiology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009000:Monocytes / Q000378:metabolism; D009504:Neutrophils; D010996:Pleural Effusion / Q000473:pathology / Q000503:physiopathology; D011552:Pseudomonas Infections / Q000150:complications* / Q000188:drug therapy*; D011550:Pseudomonas aeruginosa / Q000187:drug effects* / Q000254:growth & development / Q000472:pathogenicity / Q000502:physiology*; D011817:Rabbits; D013045:Species Specificity; D015996:Survival Rate; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D020298:U937 Cells / Q000378:metabolism; D014774:Virulence / Q000502:physiology
chemical_list: D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde