PMID- 27009697
OWN - NLM
STAT- MEDLINE
DCOM- 20170131
LR  - 20181202
IS  - 1600-0463 (Electronic)
IS  - 0903-4641 (Linking)
VI  - 124
IP  - 6
DP  - 2016 Jun
TI  - Activation of pulmonary and lymph node dendritic cells during chronic Pseudomonas 
      aeruginosa lung infection in mice.
PG  - 500-7
LID - 10.1111/apm.12530 [doi]
AB  - The majority of cystic fibrosis (CF) patients acquire chronic Pseudomonas 
      aeruginosa lung infection, resulting in increased mortality and morbidity. The 
      chronic P. aeruginosa lung infection is characterized by bacteria growing in 
      biofilm surrounded by polymorphonuclear neutrophils (PMNs). However, the 
      infection is not eradicated and the inflammatory response leads to gradual 
      degradation of the lung tissue. In CF patients, a Th2-dominated adaptive immune 
      response with a pronounced antibody response is correlated with poorer outcome. 
      Dendritic cells (DCs) are crucial in bridging the innate immune system with the 
      adaptive immune response. Once activated, the DCs deliver a set of signals to 
      uncommitted T cells that induce development, such as expansion of regulatory T 
      cells and polarization of Th1, Th2 or Th17 subsets. In this study, we 
      characterized DCs in lungs and regional lymph nodes in BALB/c mice infected using 
      intratracheal installation of P. aeruginosa embedded in seaweed alginate in the 
      lungs. A significantly elevated concentration of DCs was detected earlier in the 
      lungs than in the regional lymph nodes. To evaluate whether the chronic 
      P. aeruginosa lung infection leads to activation of DCs, costimulatory molecules 
      CD80 and CD86 were analyzed. During infection, the DCs showed significant 
      elevation of CD80 and CD86 expression in both the lungs and the regional lymph 
      nodes. Interestingly, the percentage of CD86-positive cells was significantly 
      higher than the percentage of CD80-positive cells in the lymph nodes. In 
      addition, cytokine production from Lipopolysaccharides (LPS)-stimulated DCs was 
      analyzed demonstrating elevated production of IL-6, IL-10 and IL-12. However, 
      production of IL-12 was suppressed earlier than IL-6 and IL-10. These results 
      support that DCs are involved in skewing of the Th1/Th2 balance in CF and may be 
      a possible treatment target.
CI  - (c) 2016 APMIS. Published by John Wiley & Sons Ltd.
FAU - Damlund, Dina Silke Malling
AU  - Damlund DS
AD  - Department of Clinical Microbiology, Rigshospitalet, Copenhagen, Denmark.
FAU - Christophersen, Lars
AU  - Christophersen L
AD  - Department of Clinical Microbiology, Rigshospitalet, Copenhagen, Denmark.
FAU - Jensen, Peter Ostrup
AU  - Jensen PO
AD  - Department of Clinical Microbiology, Rigshospitalet, Copenhagen, Denmark.
FAU - Alhede, Morten
AU  - Alhede M
AD  - Department of Clinical Microbiology, Rigshospitalet, Copenhagen, Denmark.
AD  - Department of International Health, Immunology and Microbiology, Faculty of 
      Health Sciences, University of Copenhagen, Copenhagen, Denmark.
FAU - Hoiby, Niels
AU  - Hoiby N
AD  - Department of Clinical Microbiology, Rigshospitalet, Copenhagen, Denmark.
FAU - Moser, Claus
AU  - Moser C
AD  - Department of Clinical Microbiology, Rigshospitalet, Copenhagen, Denmark.
LA  - eng
PT  - Journal Article
DEP - 20160324
PL  - Denmark
TA  - APMIS
JT  - APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
JID - 8803400
RN  - 0 (B7-1 Antigen)
RN  - 0 (B7-2 Antigen)
RN  - 0 (Cd86 protein, mouse)
RN  - 0 (Cytokines)
SB  - IM
MH  - Animals
MH  - B7-1 Antigen/analysis
MH  - B7-2 Antigen/analysis
MH  - Chronic Disease
MH  - Cytokines/metabolism
MH  - Dendritic Cells/chemistry/*immunology
MH  - Disease Models, Animal
MH  - Female
MH  - Lung/*pathology
MH  - Lymph Nodes/*immunology
MH  - Mice, Inbred BALB C
MH  - Pneumonia, Bacterial/*pathology
MH  - Pseudomonas Infections/*pathology
MH  - Pseudomonas aeruginosa/*immunology
OTO - NOTNLM
OT  - Pseudomonas aeruginosa
OT  - cystic fibrosis
OT  - dendritic cells
OT  - lung infection
EDAT- 2016/03/25 06:00
MHDA- 2017/02/01 06:00
CRDT- 2016/03/25 06:00
PHST- 2015/05/05 00:00 [received]
PHST- 2016/02/03 00:00 [accepted]
PHST- 2016/03/25 06:00 [entrez]
PHST- 2016/03/25 06:00 [pubmed]
PHST- 2017/02/01 06:00 [medline]
AID - 10.1111/apm.12530 [doi]
PST - ppublish
SO  - APMIS. 2016 Jun;124(6):500-7. doi: 10.1111/apm.12530. Epub 2016 Mar 24.