PMID- 11900341
OWN - NLM
STAT- MEDLINE
DCOM- 20021002
LR  - 20190916
IS  - 1073-2322 (Print)
IS  - 1073-2322 (Linking)
VI  - 17
IP  - 3
DP  - 2002 Mar
TI  - Heat stress and/or endotoxin effects on cytokine expression by human whole blood.
PG  - 217-21
AB  - Immune system cytokines induce vascular shock. Tumor necrosis factor-alpha 
      (TNF-alpha), interleukin 1beta (IL-1beta), and bacterial endotoxin (E) circulate 
      in human heatstroke to suggest that E release from a heat-damaged gut may 
      stimulate cytokines that contribute to hypovolemia. However, immune activation by 
      heat-induced tissue necrosis might stimulate cytokine generation in the absence 
      of E. To evaluate this potential and heat stress effects on the anti-inflammatory 
      cytokines, IL-1 receptor antagonist (IL-1ra) and IL-1 soluble receptor II 
      (IL-1srII), a human whole blood (HWB) model was employed in which the presence or 
      absence of E could be controlled. Using thermoelectric technology to regulate the 
      HWB heat exposures, the temperature modulations of lethal heatstroke were 
      precisely replicated (maximum temperature = 42.4 degrees C +/- 0.04 degrees C; 
      thermal area = 52.3 degrees C +/- 1.5 degrees C per min). Cytokine and mRNA 
      measurements employed enzyme-linked immunosorbant-based assay systems. 
      Significant elevations in TNF-alpha, IL-1beta, interleukin 6 (IL-6), and IL-1ra 
      resulted when HWB was exposed to E concentrations (10 ng/ml) reported to 
      circulate in heatstroke. While E-stimulated IL-1ra was significantly decreased by 
      the presence of prior heat stress (PPHS), E-stimulated IL-1beta, TNF-alpha, and 
      IL-6 were not significantly altered by PPHS, but tended to be elevated. IL-1srII 
      expression was unchanged by PPHS and/or E. PPHS in the absence of E did not 
      induce cytokine responses, nor were there elevations in TNF-alpha or IL-1beta 
      mRNA. Thus, some factor normally absent under in vitro conditions, like 
      endotoxin, was required to provoke HWB cytokine expressions and the heat stress 
      and E conditions that characterize heatstroke affected HWB cytokine metabolism to 
      favor a proinflammatory environment.
FAU - DuBose, David A
AU  - DuBose DA
AD  - Environmental Pathology/Thermal and Mountain Division, US Army Research Institute 
      of Environmental Medicine, Natick, Massachusetts 01760, USA.
FAU - Balcius, James
AU  - Balcius J
FAU - Morehouse, David
AU  - Morehouse D
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Cytokines)
RN  - 0 (Endotoxins)
RN  - 0 (IL1RN protein, human)
RN  - 0 (Interleukin 1 Receptor Antagonist Protein)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (Receptors, Interleukin-1)
RN  - 0 (Receptors, Interleukin-1 Type II)
RN  - 0 (Sialoglycoproteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Blood Cells/drug effects/*metabolism
MH  - Cells, Cultured
MH  - Cytokines/*blood
MH  - Endotoxins/immunology
MH  - Escherichia coli
MH  - Heat-Shock Response/*physiology
MH  - Humans
MH  - Interleukin 1 Receptor Antagonist Protein
MH  - Interleukin-1/blood/genetics
MH  - Interleukin-6/blood
MH  - Male
MH  - Receptors, Interleukin-1/blood
MH  - Receptors, Interleukin-1 Type II
MH  - Sialoglycoproteins/blood
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
EDAT- 2002/03/20 10:00
MHDA- 2002/10/03 04:00
CRDT- 2002/03/20 10:00
PHST- 2002/03/20 10:00 [pubmed]
PHST- 2002/10/03 04:00 [medline]
PHST- 2002/03/20 10:00 [entrez]
AID - 10.1097/00024382-200203000-00010 [doi]
PST - ppublish
SO  - Shock. 2002 Mar;17(3):217-21. doi: 10.1097/00024382-200203000-00010.