PMID- 8579760
OWN - NLM
STAT- MEDLINE
DCOM- 19960315
LR  - 20190920
IS  - 1046-7408 (Print)
IS  - 1046-7408 (Linking)
VI  - 34
IP  - 4
DP  - 1995 Oct
TI  - Regulation of human decidual cell macrophage inflammatory protein-1 alpha (MIP-1 
      alpha) production by inflammatory cytokines.
PG  - 231-5
AB  - PROBLEM: Inflammation of human gestational tissues is a key pathophysiologic 
      event in the genesis of infection-associated preterm labor. Human gestational 
      tissues produce several inflammatory cytokines after stimulation with bacterial 
      products. These include interleukin-1 beta (IL-1 beta), tumor necrosis 
      factor-alpha (TNF alpha), and IL-6. Another class of cytokines includes 
      chemokines of the "C-C" subclassification such as macrophage inflammatory 
      protein-1 alpha (MIP-1 alpha). The purpose of this study was to determine whether 
      cultured human decidual cells produce MIP-1 alpha in response to other 
      inflammatory cytokines. METHODS: Various concentrations of IL-1 beta, TNF alpha, 
      IL-6, and IL-4 were incubated with confluent monolayer cultures of decidual cells 
      isolated from normal term placentae for 16 h at 37 degrees C, and MIP-1 alpha 
      concentrations in culture supernatants were measured by ELISA. RESULTS: We found 
      that incubation of decidual cells with IL-1 beta, TNF alpha, and IL-4 resulted in 
      significant concentration-dependent increases in MIP-1 alpha production. IL-6 had 
      no effect on MIP-1 alpha production. CONCLUSIONS: Our data are the first to show 
      that human decidual cells in culture produce MIP-1 alpha in response to other 
      inflammatory cytokines. We suggest that decidual cell production of MIP-1 alpha 
      is an important early event in the pathophysiology of infection-associated 
      preterm labor.
FAU - Dudley, D J
AU  - Dudley DJ
AD  - Department of Obstetrics and Gynecology, University of Utah, School of Medicine, 
      Salt Lake City 84132, USA.
FAU - Spencer, S
AU  - Spencer S
FAU - Edwin, S
AU  - Edwin S
FAU - Mitchell, M D
AU  - Mitchell MD
LA  - eng
GR  - KO8-HD00964-03/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Denmark
TA  - Am J Reprod Immunol
JT  - American journal of reproductive immunology (New York, N.Y. : 1989)
JID - 8912860
RN  - 0 (Chemokine CCL4)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukins)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Monokines)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 207137-56-2 (Interleukin-4)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokine CCL4
MH  - Decidua/cytology/*drug effects/*metabolism
MH  - Female
MH  - Humans
MH  - Inflammation Mediators/*pharmacology
MH  - Interleukin-1/pharmacology
MH  - Interleukin-4/pharmacology
MH  - Interleukin-6/pharmacology
MH  - Interleukins/pharmacology
MH  - Macrophage Inflammatory Proteins
MH  - Monokines/*biosynthesis/*drug effects
MH  - Pregnancy
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1995/10/01 00:00
MHDA- 1995/10/01 00:01
CRDT- 1995/10/01 00:00
PHST- 1995/10/01 00:00 [pubmed]
PHST- 1995/10/01 00:01 [medline]
PHST- 1995/10/01 00:00 [entrez]
AID - 10.1111/j.1600-0897.1995.tb00946.x [doi]
PST - ppublish
SO  - Am J Reprod Immunol. 1995 Oct;34(4):231-5. doi: 
      10.1111/j.1600-0897.1995.tb00946.x.