PMID- 7865217
OWN - NLM
STAT- MEDLINE
DCOM- 19950330
LR  - 20181130
IS  - 1044-1549 (Print)
IS  - 1044-1549 (Linking)
VI  - 12
IP  - 2
DP  - 1995 Feb
TI  - Tumor necrosis factor-alpha induces mucin hypersecretion and MUC-2 gene 
      expression by human airway epithelial cells.
PG  - 196-204
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional, proinflammatory 
      cytokine that is capable of activating a diverse number of target genes within 
      multiple cell types. Little information is known regarding the role of TNF-alpha 
      in the regulation of human airway mucin hypersecretion and MUC-2 gene expression. 
      To assess the effect of TNF-alpha exposure on mucin secretion, human airway organ 
      cultures and primary cultures of human airway epithelial cells were stimulated 
      with 20 ng/ml of recombinant human TNF-alpha and mucin secretion quantitated by 
      an enzyme-linked immunosorbent assay using a specific monoclonal antibody 
      directed against human airway mucin. Significant increases in mucin secretion 
      from human airway organ cultures were initially detected at 1 h, peaked at 8 h, 
      and persisted for 24 h. The TNF-alpha-mediated mucin hypersecretion at 8 h was 
      concentration dependent. Significant increases in mucin secretion from primary 
      cultures of human airway epithelial cells were initially detected at 4 h, peaked 
      at 48 h, and persisted for 72 h after stimulation with 20 ng/ml of recombinant 
      human TNF-alpha. The TNF-alpha-mediated mucin hypersecretion at 48 h from primary 
      cultures of human airway epithelial cells was inhibited by coincubation with 
      soluble 55 kD, type I TNF receptors. Using reverse transcription-polymerase chain 
      reaction and a human pulmonary mucoepidermoid carcinoma cell line (NCI-H292), 
      increases in MUC-2 steady-state mRNA levels were first detectable after 30 min of 
      TNF-alpha stimulation and persisted for 24 h. Cycloheximide did not inhibit 
      TNF-alpha-mediated MUC-2 mRNA expression at 1 h, suggesting that new protein 
      translation was not required.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Levine, S J
AU  - Levine SJ
AD  - Critical Care Medicine Department, Warren G. Magnuson Clinical Center, National 
      Institutes of Health, Bethesda, Maryland 20892-1662.
FAU - Larivee, P
AU  - Larivee P
FAU - Logun, C
AU  - Logun C
FAU - Angus, C W
AU  - Angus CW
FAU - Ognibene, F P
AU  - Ognibene FP
FAU - Shelhamer, J H
AU  - Shelhamer JH
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Am J Respir Cell Mol Biol
JT  - American journal of respiratory cell and molecular biology
JID - 8917225
RN  - 0 (Actins)
RN  - 0 (DNA Primers)
RN  - 0 (MUC2 protein, human)
RN  - 0 (Mucin-2)
RN  - 0 (Mucins)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
GS  - MUC-2
MH  - Actins/genetics
MH  - Base Sequence
MH  - Cells, Cultured
MH  - DNA Primers/genetics
MH  - Epithelium/drug effects/metabolism
MH  - Gene Expression/drug effects
MH  - Humans
MH  - Molecular Sequence Data
MH  - Mucin-2
MH  - Mucins/*genetics/*metabolism
MH  - Organ Culture Techniques
MH  - Recombinant Proteins/pharmacology
MH  - Respiratory System/*drug effects/metabolism
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1995/02/01 00:00
MHDA- 1995/02/01 00:01
CRDT- 1995/02/01 00:00
PHST- 1995/02/01 00:00 [pubmed]
PHST- 1995/02/01 00:01 [medline]
PHST- 1995/02/01 00:00 [entrez]
AID - 10.1165/ajrcmb.12.2.7865217 [doi]
PST - ppublish
SO  - Am J Respir Cell Mol Biol. 1995 Feb;12(2):196-204. doi: 
      10.1165/ajrcmb.12.2.7865217.