PMID- 8821103
OWN - NLM
STAT- MEDLINE
DCOM- 19961106
LR  - 20190914
IS  - 1073-2322 (Print)
IS  - 1073-2322 (Linking)
VI  - 5
IP  - 1
DP  - 1996 Jan
TI  - Bacterial ingestion, tumor necrosis factor-alpha, and heat induce programmed cell 
      death in activated neutrophils.
PG  - 47-51
AB  - Resolution of acute inflammation requires the removal of sequestered neutrophils 
      (PMN) from the inflammatory site by apoptosis and ingestion by tissue 
      macrophages; however, sequestered PMN are prevented from undergoing programmed 
      cell death by some of the mediators of the acute inflammatory process, including 
      lipopolysaccharide (LPS), granulocyte-macrophage colony-stimulating factor, and 
      interleukin 2. This delay in apoptosis could lead to necrosis resulting in tissue 
      damage. Tumor necrosis factor-alpha (TNF-alpha), Escherichia coli ingestion 
      resulting in a respiratory burst, and heat have been shown to induce PMN 
      apoptosis. The effects of TNF-alpha, E. coli ingestion, and heat shock on the one 
      hand and LPS on the other, on PMN apoptosis are unknown. The aim of this study 
      was to determine if TNF-alpha, E. coli ingestion, and heat shock, which have been 
      shown to induce PMN apoptosis, could override the delay in apoptosis associated 
      with LPS. PMN (10(6)) isolated from 10 healthy volunteers were cultured in either 
      medium alone or PMN cultured with LPS (10 ng/mL/1 h). PMN activation was assessed 
      subsequently by phagocytosis of E. coli and CD11b expression. PMN were then 
      further studied under four culture conditions: medium alone, TNF-alpha (100 
      U/mL), E. coli (1:25, PMN:E. coli), and heat shock (42 degrees C for 45 min). 
      Apoptosis was assessed over time by propidium iodide staining of DNA and Fc gamma 
      RIII receptor expression. The results demonstrate, for the first time, that the 
      mechanisms by which LPS delays PMN apoptosis are overridden by the mechanisms by 
      which TNF-alpha, E. coli ingestion, and heat shock induce programmed cell death. 
      Factors regulating PMN apoptosis have an important role to play in the resolution 
      of acute inflammation. Identification of these factors and their interaction have 
      important implications for the development of therapeutic strategies aimed at 
      modulating the acute inflammatory response.
FAU - Watson, R W
AU  - Watson RW
AD  - Department of Surgery, Royal College of Surgeons in Ireland, Dublin.
FAU - Redmond, H P
AU  - Redmond HP
FAU - Wang, J H
AU  - Wang JH
FAU - Bouchier-Hayes, D
AU  - Bouchier-Hayes D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Apoptosis/drug effects/*physiology
MH  - Escherichia coli
MH  - Evaluation Studies as Topic
MH  - *Hot Temperature
MH  - Humans
MH  - Inflammation/*pathology
MH  - Lipopolysaccharides/pharmacology
MH  - Neutrophil Activation/*physiology
MH  - Phagocytosis/*physiology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1996/01/01 00:00
MHDA- 1996/01/01 00:01
CRDT- 1996/01/01 00:00
PHST- 1996/01/01 00:00 [pubmed]
PHST- 1996/01/01 00:01 [medline]
PHST- 1996/01/01 00:00 [entrez]
AID - 10.1097/00024382-199601000-00010 [doi]
PST - ppublish
SO  - Shock. 1996 Jan;5(1):47-51. doi: 10.1097/00024382-199601000-00010.