PMID- 8967504
OWN - NLM
STAT- MEDLINE
DCOM- 19961206
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 270
IP  - 5 Pt 1
DP  - 1996 May
TI  - Tumor necrosis factor-alpha decreases surfactant protein B mRNA in murine lung.
PG  - L714-21
AB  - Respiratory failure secondary to acute lung inflammation is associated with 
      quantitative and qualitative abnormalities of pulmonary surfactant. The 
      surfactant-associated proteins (SP)-A, -B, and -C are critical for normal 
      surfactant function, synthesis, and metabolism. Tumor necrosis factor-alpha 
      (TNF-alpha), a primary mediator of acute lung inflammation, decreased SP gene 
      expression in vitro (32, 34). In the present in vivo study, transient T cell 
      activation and TNF-alpha release were initiated by intraperitoneal administration 
      of anti-CD3 antibody 145-2C11. Serum TNF-alpha was elevated 2 h after injection 
      of the antibody. SP-B and -C mRNA were decreased 12 and 24 h after antibody 
      treatment. Intratracheal murine TNF-alpha also resulted in decreased SP-B and 
      SP-C mRNA levels in the bronchiolar and alveolar epithelium of adult FVB/N mice, 
      as demonstrated by S1 nuclease protection and in situ hybridization assays, 
      despite minimal histological inflammation. SP-A mRNA was not significantly 
      altered after anti-CD3 antibody and was only mildly decreased after TNF-alpha. As 
      previously reported, intercellular adhesion molecule-1 mRNA was elevated after 
      intratracheal TNF-alpha. SP insufficiency contributes to the pathogenesis of 
      pulmonary diseases associated with increased TNF-alpha, such as adult respiratory 
      distress syndrome and pneumonia (8). TNF-alpha-mediated decrease in SP gene 
      expression may contribute to the surfactant dysfunction and atelectasis observed 
      in inflammatory lung diseases.
FAU - Pryhuber, G S
AU  - Pryhuber GS
AD  - Division of Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, 
      Ohio 45229, USA.
FAU - Bachurski, C
AU  - Bachurski C
FAU - Hirsch, R
AU  - Hirsch R
FAU - Bacon, A
AU  - Bacon A
FAU - Whitsett, J A
AU  - Whitsett JA
LA  - eng
GR  - HD-07200/HD/NICHD NIH HHS/United States
GR  - HL-38859/HL/NHLBI NIH HHS/United States
GR  - HL-41496/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Antibodies)
RN  - 0 (CD3 Complex)
RN  - 0 (Proteolipids)
RN  - 0 (Pulmonary Surfactant-Associated Protein A)
RN  - 0 (Pulmonary Surfactant-Associated Proteins)
RN  - 0 (Pulmonary Surfactants)
RN  - 0 (RNA, Messenger)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Animals
MH  - Antibodies/immunology/pharmacology
MH  - CD3 Complex/immunology
MH  - Cricetinae
MH  - Female
MH  - Humans
MH  - Injections, Intraperitoneal
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - Lung/*metabolism
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Proteolipids/*genetics
MH  - Pulmonary Surfactant-Associated Protein A
MH  - Pulmonary Surfactant-Associated Proteins
MH  - Pulmonary Surfactants/*genetics
MH  - RNA, Messenger/*antagonists & inhibitors/metabolism
MH  - Recombinant Proteins
MH  - Trachea
MH  - Tumor Necrosis Factor-alpha/administration & dosage/analysis/*pharmacology
EDAT- 1996/05/01 00:00
MHDA- 1996/05/01 00:01
CRDT- 1996/05/01 00:00
PHST- 1996/05/01 00:00 [pubmed]
PHST- 1996/05/01 00:01 [medline]
PHST- 1996/05/01 00:00 [entrez]
AID - 10.1152/ajplung.1996.270.5.L714 [doi]
PST - ppublish
SO  - Am J Physiol. 1996 May;270(5 Pt 1):L714-21. doi: 10.1152/ajplung.1996.270.5.L714.