PMID- 16026013
OWN - NLM
STAT- MEDLINE
DCOM- 20050815
LR  - 20201209
IS  - 0341-2040 (Print)
IS  - 0341-2040 (Linking)
VI  - 183
IP  - 2
DP  - 2005 Mar-Apr
TI  - Alterations of adhesion molecule expression and inflammatory mediators in acute 
      lung injury induced by septic and non-septic challenges.
PG  - 87-100
AB  - The lung is frequently the first failing organ during the sequential development 
      of multiple organ dysfunction under both septic or non-septic conditions. The 
      present study compared polymorphisms of tumor necrosis factor (TNFalpha), 
      monocyte chemoattractant protein-1 (MCP-1), and adhesion molecule (AM) expression 
      on circulating, recruited, and migrating leukocytes in the development of lung 
      injury after induction of acute pancreatitis (AP) or abdominal sepsis by cecal 
      ligation and puncture (CLP). Pulmonary alveolar barrier and endothelial barrier 
      permeability dysfunction were measured. The expression of AMs (CD11b, CD11b/c, 
      CD31, CD54 and CD62L) on leukocytes isolated from blood, lung tissue, and 
      bronchoalveolar space were measured by flowcytometry. Plasma exudation to the 
      interstitial tissue and the bronchoalveolar space significantly increased 1 and 3 
      hours after induction of pancreatitis and to the bronchoalveolar space from 6 
      hours after sepsis. Bronchoalveolar levels of MCP-1 significantly increased 
      earlier than plasma exudation to the alveoli in both pancreatitis and sepsis. 
      Alterations in expression of adhesion molecules on bronchoalveolar lavage (BAL) 
      leukocytes can represent a marker reflecting leukocyte activation in the lung 
      tissue, since both BAL and lung tissue leukocytes showed similar patterns of 
      changes. Expression of adhesion molecules on circulating leukocytes increased 1 
      hour after induction of pancreatitis. Activating phenotypes of circulating, lung 
      tissue and bronchoalveolar leukocytes may thus be responsible for the-development 
      and severity of secondary lung injury.
FAU - Zhao, Xia
AU  - Zhao X
AD  - Department of Surgery, Lund University, Lund, Sweden.
FAU - Dib, Marwan
AU  - Dib M
FAU - Andersson, Ellen
AU  - Andersson E
FAU - Shi, Changbin
AU  - Shi C
FAU - Widegren, Bengt
AU  - Widegren B
FAU - Wang, Xiangdong
AU  - Wang X
FAU - Andersson, Roland
AU  - Andersson R
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Lung
JT  - Lung
JID - 7701875
RN  - 0 (Antigens, CD)
RN  - 0 (CD11 Antigens)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Antigens, CD/metabolism
MH  - CD11 Antigens/metabolism
MH  - Cell Adhesion Molecules/*metabolism
MH  - Chemokine CCL2/genetics
MH  - Flow Cytometry
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - Interleukin-6/*metabolism
MH  - Leukocytes
MH  - Male
MH  - Multiple Organ Failure/metabolism
MH  - Pancreatitis/physiopathology
MH  - Polymorphism, Genetic
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Respiratory Distress Syndrome/*metabolism
MH  - Tumor Necrosis Factor-alpha/*genetics
EDAT- 2005/07/20 09:00
MHDA- 2005/08/16 09:00
CRDT- 2005/07/20 09:00
PHST- 2005/07/20 09:00 [pubmed]
PHST- 2005/08/16 09:00 [medline]
PHST- 2005/07/20 09:00 [entrez]
AID - 10.1007/s00408-004-2522-3 [doi]
PST - ppublish
SO  - Lung. 2005 Mar-Apr;183(2):87-100. doi: 10.1007/s00408-004-2522-3.