PMID- 10069998
OWN - NLM
STAT- MEDLINE
DCOM- 19990415
LR  - 20190205
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 276
IP  - 3
DP  - 1999 Mar
TI  - Chemokine expression in CF epithelia: implications for the role of CFTR in RANTES 
      expression.
PG  - C700-10
LID - 10.1152/ajpcell.1999.276.3.C700 [doi]
AB  - To delineate the mechanisms that facilitate leukocyte migration into the cystic 
      fibrosis (CF) lung, expression of chemokines, including interleukin-8 (IL-8), 
      monocyte chemoattractant protein-1 (MCP-1), and RANTES, was compared between CF 
      and non-CF airway epithelia. The findings presented herein demonstrate that, 
      under either basal conditions or tumor necrosis factor-alpha (TNF-alpha)- and/or 
      interferon-gamma (IFN-gamma)-stimulated conditions, a consistent pattern of 
      differences in the secretion of IL-8 and MCP-1 between CF and non-CF epithelial 
      cells was not observed. In contrast, CF epithelial cells expressed no detectable 
      RANTES protein or mRNA under basal conditions or when stimulated with TNF-alpha 
      and/or IFN-gamma (P </= 0.05), unlike their non-CF counterparts. Correction of 
      the CF transmembrane conductance regulator (CFTR) defect in CF airway epithelial 
      cells restored the induction of RANTES protein and mRNA by TNF-alpha in 
      combination with IFN-gamma (P </= 0.05) but had little effect on IL-8 or MCP-1 
      production compared with mock controls. Transfection studies utilizing RANTES 
      promoter constructs suggested that CFTR activates the RANTES promoter via a 
      nuclear factor-kappaB-mediated pathway. Together, these results suggest that 1) 
      RANTES expression is altered in CF epithelia and 2) epithelial expression of 
      RANTES, but not IL-8 or MCP-1, is dependent on CFTR.
FAU - Schwiebert, L M
AU  - Schwiebert LM
AD  - Department of Physiology and Biophysics, University of Alabama, Birmingham, 
      Alabama 35294, USA.
FAU - Estell, K
AU  - Estell K
FAU - Propst, S M
AU  - Propst SM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (CFTR protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Chemokines)
RN  - 0 (Drug Combinations)
RN  - 0 (Interleukin-8)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Bronchi/drug effects/*metabolism/pathology
MH  - Chemokine CCL2/metabolism
MH  - Chemokine CCL5/genetics/*metabolism
MH  - Chemokines/*metabolism
MH  - Cystic Fibrosis/*metabolism
MH  - Cystic Fibrosis Transmembrane Conductance Regulator/*physiology
MH  - Drug Combinations
MH  - Epithelial Cells/drug effects/metabolism
MH  - Humans
MH  - Interferon-gamma/pharmacology
MH  - Interleukin-8/metabolism
MH  - Pancreatic Neoplasms/metabolism/pathology
MH  - Promoter Regions, Genetic/physiology
MH  - RNA, Messenger/metabolism
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1999/03/10 00:00
MHDA- 1999/03/10 00:01
CRDT- 1999/03/10 00:00
PHST- 1999/03/10 00:00 [pubmed]
PHST- 1999/03/10 00:01 [medline]
PHST- 1999/03/10 00:00 [entrez]
AID - 10.1152/ajpcell.1999.276.3.C700 [doi]
PST - ppublish
SO  - Am J Physiol. 1999 Mar;276(3):C700-10. doi: 10.1152/ajpcell.1999.276.3.C700.