PMID- 12842853
OWN - NLM
STAT- MEDLINE
DCOM- 20040116
LR  - 20220317
IS  - 1073-449X (Print)
IS  - 1073-449X (Linking)
VI  - 168
IP  - 9
DP  - 2003 Nov 1
TI  - Functional identification of the alveolar edema reabsorption activity of murine 
      tumor necrosis factor-alpha.
PG  - 1043-50
AB  - Tumor necrosis factor-alpha (TNF-alpha) activates sodium channels in Type II 
      alveolar epithelial cells, an important mechanism for the reported fluid 
      resorption capacity of the cytokine. Both TNF-alpha receptor-dependent and 
      -independent effects were proposed for this activity in vitro, the latter 
      mechanism mediated by the lectin-like domain of the molecule. In this study, the 
      relative contribution of the receptor-dependent versus receptor-independent 
      activities was investigated in an in situ mouse lung model and an ex vivo rat 
      lung model. Fluid resorption due to murine TNF-alpha (mTNF-alpha) was functional 
      in mice that were genetically deficient in both types of mTNF-alpha receptor, 
      establishing the importance of mTNF-alpha receptor-independent effects in this 
      species. In addition, we assessed the capacity of an mTNF-alpha-derived peptide 
      (mLtip), which activates sodium transport by a receptor-independent mechanism, to 
      reduce lung water content in an isolated, ventilated, autologous blood-perfused 
      rat lung model. The results show that in this model, mLtip, in contrast to 
      mTNF-alpha, produced a progressive recovery of dynamic lung compliance and airway 
      resistance after alveolar flooding. There was also a significant reduction in 
      lung water. These results indicate that the receptor-independent lectin-like 
      domain of mTNF-alpha has a potential physiological role in the resolution of 
      alveolar edema in rats and mice.
FAU - Elia, Nadia
AU  - Elia N
AD  - Division of Anesthesiological Investigations, University Medical Center, Geneva, 
      Switzerland.
FAU - Tapponnier, Maxime
AU  - Tapponnier M
FAU - Matthay, Michael A
AU  - Matthay MA
FAU - Hamacher, Jurg
AU  - Hamacher J
FAU - Pache, Jean-Claude
AU  - Pache JC
FAU - Brundler, Marie-Anne
AU  - Brundler MA
FAU - Totsch, Martin
AU  - Totsch M
FAU - De Baetselier, Patrick
AU  - De Baetselier P
FAU - Fransen, Lucie
AU  - Fransen L
FAU - Fukuda, Norimasa
AU  - Fukuda N
FAU - Morel, Denis R
AU  - Morel DR
FAU - Lucas, Rudolf
AU  - Lucas R
LA  - eng
GR  - HL51854/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20030703
PL  - United States
TA  - Am J Respir Crit Care Med
JT  - American journal of respiratory and critical care medicine
JID - 9421642
RN  - 0 (Diuretics)
RN  - 0 (Peptide Fragments)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Sodium Channels)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 7DZO8EB0Z3 (Amiloride)
SB  - IM
CIN - Am J Respir Crit Care Med. 2003 Nov 1;168(9):1022-3. PMID: 14581284
MH  - Amiloride/pharmacology
MH  - Animals
MH  - Biological Transport/physiology
MH  - Diuretics/pharmacology
MH  - Female
MH  - Lung/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Models, Animal
MH  - Organ Size
MH  - Peptide Fragments/metabolism
MH  - Pulmonary Edema/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Tumor Necrosis Factor/deficiency/metabolism
MH  - Respiratory Mechanics/drug effects
MH  - Sodium Channels/drug effects/metabolism
MH  - Tumor Necrosis Factor-alpha/*metabolism
EDAT- 2003/07/05 05:00
MHDA- 2004/01/17 05:00
CRDT- 2003/07/05 05:00
PHST- 2003/07/05 05:00 [pubmed]
PHST- 2004/01/17 05:00 [medline]
PHST- 2003/07/05 05:00 [entrez]
AID - 200206-618OC [pii]
AID - 10.1164/rccm.200206-618OC [doi]
PST - ppublish
SO  - Am J Respir Crit Care Med. 2003 Nov 1;168(9):1043-50. doi: 
      10.1164/rccm.200206-618OC. Epub 2003 Jul 3.