PMID- 20042672
OWN - NLM
STAT- MEDLINE
DCOM- 20100316
LR  - 20211020
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Print)
IS  - 0002-9440 (Linking)
VI  - 176
IP  - 2
DP  - 2010 Feb
TI  - Plasmacytoid dendritic cells control lung inflammation and monocyte recruitment 
      in indirect acute lung injury in mice.
PG  - 764-73
LID - 10.2353/ajpath.2010.090765 [doi]
AB  - Indirect acute lung injury (ALI, not caused by a direct insult to the lung) 
      represents the first organ dysfunction in trauma patients, with nonpulmonary 
      sepsis being the most common cause of indirect ALI. Dendritic cells (DCs) are 
      thought to participate in a number of inflammatory lung diseases; however, their 
      role in indirect ALI is currently not established. Using a clinically relevant 
      model of indirect ALI induced in mice by hemorrhagic shock followed 24 hours 
      later by polymicrobial septic challenge, we report that mature DC numbers were 
      markedly increased in the lung during indirect ALI. DC depletion induced a 
      significant increase in indirect ALI severity, which was associated with enhanced 
      lung and plasma proinflammatory cytokine concentration and recruitment of 
      proinflammatory CD115(+) monocytes in response to increased lung monocyte 
      chemotactic protein-1 production. Among the different DC subpopulations, 
      plasmacytoid DCs, which were induced and activated in the lung during indirect 
      ALI, were responsible for this effect because their specific depletion reproduced 
      the observations made in DC-depleted mice. As the recruitment of monocytes to the 
      lung plays a central deleterious role in the pathophysiology of indirect ALI, our 
      data therefore position plasmacytoid DCs as important regulators of acute lung 
      inflammation.
FAU - Venet, Fabienne
AU  - Venet F
AD  - Division of Surgical Research, Rhode Island Hospital/Brown University, 
      Providence, RI 02903, USA.
FAU - Huang, Xin
AU  - Huang X
FAU - Chung, Chun-Shiang
AU  - Chung CS
FAU - Chen, Yaping
AU  - Chen Y
FAU - Ayala, Alfred
AU  - Ayala A
LA  - eng
GR  - R01 HL073525/HL/NHLBI NIH HHS/United States
GR  - S10 RR021051/RR/NCRR NIH HHS/United States
GR  - R01 HL73525/HL/NHLBI NIH HHS/United States
GR  - 1S10RR021051-01A2/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20091230
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Hbegf protein, mouse)
RN  - 0 (Heparin-binding EGF-like Growth Factor)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Nectins)
SB  - IM
MH  - Acute Lung Injury/complications/genetics/immunology/*pathology
MH  - Animals
MH  - Cell Adhesion Molecules/genetics
MH  - Cell Count
MH  - Cells, Cultured
MH  - Chemotaxis, Leukocyte/*physiology
MH  - Dendritic Cells/pathology/*physiology
MH  - Disease Models, Animal
MH  - Heparin-binding EGF-like Growth Factor
MH  - Intercellular Signaling Peptides and Proteins/genetics
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Monocytes/pathology/*physiology
MH  - Nectins
MH  - Pneumonia/etiology/genetics/*immunology/pathology
MH  - Severity of Illness Index
PMC - PMC2808083
EDAT- 2010/01/01 06:00
MHDA- 2010/03/17 06:00
PMCR- 2011/02/01
CRDT- 2010/01/01 06:00
PHST- 2010/01/01 06:00 [entrez]
PHST- 2010/01/01 06:00 [pubmed]
PHST- 2010/03/17 06:00 [medline]
PHST- 2011/02/01 00:00 [pmc-release]
AID - S0002-9440(10)60390-2 [pii]
AID - 10.2353/ajpath.2010.090765 [doi]
PST - ppublish
SO  - Am J Pathol. 2010 Feb;176(2):764-73. doi: 10.2353/ajpath.2010.090765. Epub 2009 
      Dec 30.