title: Luminescent-activated transfected killer cells to monitor leukocyte trafficking during systemic bacterial and fungal infection.
abstract: BACKGROUND
  Activated transfected killer (ATAK) cells are immortal phagocytes transfected with a luminescence reporter that effectively treat lethal infections in neutropenic mice. Their in vivo trafficking, lifespan, and immunogenicity are unknown.
  
  
  METHODS
  Mice were made neutropenic; infected or not with Staphylococcus aureus, Acinetobacter baumannii, Candida albicans, or Aspergillus fumigatus; and treated intraperitoneally with ATAK cells. Cell trafficking and lifespan were assessed by in vivo imaging and reverse transcription-polymerase chain reaction.
  
  
  RESULTS
  In uninfected neutropenic mice, ATAK cells spread from the mesentery into visceral organs on days 1-3. Splenic accumulation of ATAK cells increased at day 1 after infection with S. aureus and A. baumannii, and kidney accumulation increased in mice infected with C. albicans. Lung accumulation was seen at day 3 in mice infected by inhalation with A. fumigatus. By day 8, coincident with increasing anti-ATAK antibodies, luminescence signal was lost and there was no detectable mRNA transcription from ATAK cells.
  
  
  CONCLUSIONS
  ATAK cells accumulated in target organs with distinct profiles, depending on the microbial etiology of infection. Finally, generation of an anti-ATAK immune response may provide an important safety mechanism that helps clear the cells from the host as the marrow recovers.
authors: Department of Medicine, Division of General Internal Medicine, Los Angeles Biomedical Research Institute, Harbor-University of California at Los Angeles Medical Center, Torrance, CA, USA.
authors: Lin
authors: L
authors: Lin
authors: Ashraf S
authors: AS
authors: Ibrahim
authors: Beverlie
authors: B
authors: Baquir
authors: Andrew
authors: A
authors: Palosaari
authors: Brad
authors: B
authors: Spellberg
mesh_terms: D000151:Acinetobacter Infections / Q000276:immunology* / Q000382:microbiology / Q000628:therapy; D040981:Acinetobacter baumannii; D000818:Animals; D001232:Aspergillus fumigatus; D002176:Candida albicans; D002177:Candidiasis / Q000276:immunology* / Q000382:microbiology / Q000628:therapy; D003520:Cyclophosphamide; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000235:genetics; D018922:HL-60 Cells; D006801:Humans; D016219:Immunotherapy, Adoptive; D007668:Kidney / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology*; D049449:Luminescence; D008168:Lung / Q000276:immunology; D008213:Lymphocyte Activation; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009503:Neutropenia / Q000139:chemically induced; D055732:Pulmonary Aspergillosis / Q000276:immunology* / Q000382:microbiology / Q000628:therapy; D012333:RNA, Messenger / Q000378:metabolism*; D013154:Spleen / Q000276:immunology; D013203:Staphylococcal Infections / Q000276:immunology* / Q000382:microbiology / Q000628:therapy; D013211:Staphylococcus aureus; D013937:Thymidine Kinase / Q000235:genetics; D013997:Time Factors; D014162:Transfection
chemical_list: D012333:RNA, Messenger; D003520:Cyclophosphamide; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D013937:Thymidine Kinase