Mycobacterial cell wall components induce the production of TNF-α, IL-1, and IL-6 by bovine monocytes and the murine macrophage cell line RAW 264.7

1994 ◽  
Vol 16 (6) ◽  
pp. 401-411 ◽  
Author(s):  
Jeffrey L. Adams ◽  
Charles J. Czuprynski
BioTechniques ◽  
1999 ◽  
Vol 27 (4) ◽  
pp. 824-832 ◽  
Author(s):  
C.D. Thompson ◽  
M.R. Frazier-Jessen ◽  
R. Rawat ◽  
R.P. Nordan ◽  
R.T. Brown

The Analyst ◽  
2018 ◽  
Vol 143 (14) ◽  
pp. 3489-3498 ◽  
Author(s):  
J. Dybas ◽  
M. Grosicki ◽  
M. Baranska ◽  
K. M. Marzec

Herein, we provide the Raman imaging results for different stages of erythrophagocytosis of senescent red blood cells executed by isolated murine primary Kupffer cells and a murine macrophage cell line (RAW 264.7).


2001 ◽  
Vol 69 (5) ◽  
pp. 3214-3223 ◽  
Author(s):  
Xiaohan Du ◽  
Martin G. Low

ABSTRACT Serum glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) activity is reduced over 75% in systemic inflammatory response syndrome. To investigate the mechanism of this response, expression of the GPI-PLD gene was studied in the mouse monocyte-macrophage cell line RAW 264.7 stimulated with lipopolysaccharide (LPS; 0.5 to 50 ng/ml). GPI-PLD mRNA was reduced approximately 60% in a time- and dose-dependent manner. Oxidative stress induced by 0.5 mM H2O2 or 50 μM menadione also caused a greater than 50% reduction in GPI-PLD mRNA. The antioxidant N-acetyl-l-cysteine attenuated the down-regulatory effect of H2O2but not of LPS. Cotreatment of the cells with actinomycin D inhibited down-regulation induced by either LPS or H2O2. The half-life of GPI-PLD mRNA was not affected by LPS, or decreased slightly with H2O2, indicating that the reduction in GPI-PLD mRNA is due primarily to transcriptional regulation. Stimulation with tumor necrosis factor alpha (TNF-α) resulted in ∼40% reduction in GPI-PLD mRNA in human A549 alveolar carcinoma cells but not RAW 264.7 cells, suggesting that alternative pathways could exist in different cell types for down-regulating GPI-PLD expression during an inflammatory response and the TNF-α autocrine signaling mechanism alone is not sufficient to recapitulate the LPS-induced reduction of GPI-PLD in macrophages. Sublines of RAW 264.7 cells with reduced GPI-PLD expression exhibited increased cell sensitivity to LPS stimulation and membrane-anchored CD14 expression on the cell surface. Our data suggest that down-regulation of GPI-PLD could play an important role in the control of proinflammatory responses.


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