PMID- 1327012
OWN - NLM
STAT- MEDLINE
DCOM- 19921102
LR  - 20131121
IS  - 1044-1549 (Print)
IS  - 1044-1549 (Linking)
VI  - 7
IP  - 4
DP  - 1992 Oct
TI  - Tumor necrosis factor-alpha and interleukin-1 alpha synergistically enhance 
      phorbol myristate acetate-induced superoxide production by rat bone 
      marrow-derived macrophages.
PG  - 379-84
AB  - Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha) are 
      secreted by macrophages in response to endotoxin challenge. In addition, 
      macrophages express receptors for both of these cytokines. Macrophage function 
      can therefore be modulated by regulation of both cytokine production and receptor 
      levels. We have initiated studies to investigate the effects of TNF-alpha and 
      IL-1 alpha on macrophage function. Macrophages were obtained by in vitro 
      differentiation of rat bone marrow cells. The biologic response to TNF-alpha and 
      IL-1 alpha was assessed by measurement of superoxide production quantitated by 
      the reduction of cytochrome c in response to phorbol myristate acetate. 
      Macrophages were treated with endotoxin (LPS), TNF-alpha, and IL-1 alpha, alone 
      and in combination. None of these agents was a primary stimulus for superoxide 
      production. However, after treatment with endotoxin or TNF-alpha for 24 h, 
      macrophages were primed for enhanced production of superoxide. The priming effect 
      of LPS was due, at least in part, to endogenously produced TNF-alpha, since 
      anti-murine TNF-alpha antibodies blocked the LPS-mediated priming by 
      approximately 30%. IL-1 alpha did not prime macrophages, but treatment with IL-1 
      alpha followed by TNF-alpha or LPS resulted in enhanced superoxide production. 
      IL-1 alpha treatment of macrophages resulted in an increase in TNF-alpha 
      receptors, which might explain the synergistic priming of TNF-alpha and IL-1 
      alpha.
FAU - Tanner, W G
AU  - Tanner WG
AD  - Department of Veterans Affairs, Vanderbilt University, Nashville, Tennessee.
FAU - Welborn, M B
AU  - Welborn MB
FAU - Shepherd, V L
AU  - Shepherd VL
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Am J Respir Cell Mol Biol
JT  - American journal of respiratory cell and molecular biology
JID - 8917225
RN  - 0 (Antibodies)
RN  - 0 (Cytochrome c Group)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 11062-77-4 (Superoxides)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Animals
MH  - Antibodies
MH  - Bone Marrow/*metabolism
MH  - Cells, Cultured
MH  - Cytochrome c Group/metabolism
MH  - Drug Synergism
MH  - Interleukin-1/*pharmacology
MH  - Kinetics
MH  - Lipopolysaccharides/pharmacology
MH  - Macrophages/drug effects/*metabolism
MH  - Rats
MH  - Recombinant Proteins/pharmacology
MH  - Superoxides/*metabolism
MH  - Tetradecanoylphorbol Acetate/*pharmacology
MH  - Tumor Necrosis Factor-alpha/immunology/*pharmacology
EDAT- 1992/10/01 00:00
MHDA- 1992/10/01 00:01
CRDT- 1992/10/01 00:00
PHST- 1992/10/01 00:00 [pubmed]
PHST- 1992/10/01 00:01 [medline]
PHST- 1992/10/01 00:00 [entrez]
AID - 10.1165/ajrcmb/7.4.379 [doi]
PST - ppublish
SO  - Am J Respir Cell Mol Biol. 1992 Oct;7(4):379-84. doi: 10.1165/ajrcmb/7.4.379.