Expression of intracellular cytokine cascade, HSP72 and apoptosis in monocyte subsets during exertional heat stress in trained and untrained individuals

PDF

Authors
  1. Selkirk, G.A.
  2. McLellan, T.M.
  3. Wright, H.E.
  4. Rhind, S.G.
Corporate Authors
Defence R&D Canada - Toronto, Toronto ONT (CAN);York Univ, Toronto ONT (CAN)
Abstract
This study examined intracellular cytokine, heat shock protein (HSP) 72 and cellular apoptosis in classical and inflammatory CD14+ monocyte subsets during exertional heat stress (EHS). Subjects were divided into trained (TR, n=12, = 70 ± 2 mL•kgLBM-1•min-1) and untrained (UT, n=11, = 50 ± 1 mL•kgLBM-1•min-1) groups prior to walking at 4.5 km•h-1 with 2% elevation in a climatic chamber (40°C; 30% R.H.), wearing protective clothing until exhaustion (Exh). Venous blood samples at baseline and 0.5°C rectal temperature increments (38.0°C, 38.5°C, 39.0°C, 39.5°C and 40.0°C/Exh) were analyzed for icytokine (TNF-α, IL-1β, IL-6, IL-1ra and IL-10) in CD14++CD16-/CD14+CD16+ and HSP72/Apoptosis in CD14Bri/CDDim subsets. In addition, serum levels of extracellular (e) HSP72 were also examined. Baseline and Exh samples were separately stimulated with LPS (1 µg•mL-1), heat shocked (42°C) and cultured in vitro for 2 hours. A greater temperature dependent increase in CD14+CD16+ cells was observed in TR compared to UT as well as a greater LPS tolerance following in vitro LPS stimulation. TNF-α and IL-1β cytokine expression was elevated in CD14+CD16+ but not in CD14++CD16- cells. Greater intracellular HSP72 inducibility and eHSP72 was observed in TR compared to UT, which coincided with a reduced apoptosis at Exh and following in vitro heat shock, however, HSP inducibility did not appear uniform across CD14+ subsets. Findings suggest circulating CD14+C

Il y a un résumé en français ici.

Keywords
intracellular cytokines, immune function, cardiovascular/thermoregulatory strain
Report Number
DRDC-TORONTO-SL-2008-140 — Scientific Literature
Date of publication
21 Jan 2009
Number of Pages
12
Reprinted from
American Journal of Physiology: Regulatory, Integrative and Comparitive Physiology, no 296, 2009, p R575-R586
DSTKIM No
CA032290
CANDIS No
531406
Format(s):
Electronic Document(PDF)

Permanent link

Document 1 of 1

Date modified: