0
Abstract: Slide Presentations |

EFFECT OF TEMPERATURE ON SUPEROXIDE PRODUCTION BY THP1 MONOCYTES FREE TO VIEW

Victor K. Salloum, MD*; Saikat Chakraborty, PhD; Akhil Bidani, MD
Author and Funding Information

UT Health Science Center, Houston, TX


Chest


Chest. 2005;128(4_MeetingAbstracts):166S. doi:10.1378/chest.128.4_MeetingAbstracts.166S-a
Text Size: A A A
Published online

Abstract

PURPOSE:  The respiratory burst of immune cells is an integral part of host defense. In this study, we investigate the effect of temperature (between 25°C and 42°C) on the dynamics of superoxide (O2-) production during the respiratory burst in PMA-activated THP-1 monocytes.

METHODS:  The dynamics of superoxide production of PMA-activated monocytes is measured at each temperature (between 25°C and 42°C) as the superoxide dismutase-inhibitable reduction of cytochrome c using the classical spectrophotometric assay.

RESULTS:  At each temperature, the cumulative O2- concentration shows a lag period with low O2- production, followed by a period of accelerated production and then a slow saturation to a steady state concentration. Our measurements show that both the dynamics of O2- production and the maximum amount of O2- produced at steady state are affected by temperature, with the latter being affected more profoundly. The steady state O2- concentration shows a triphasic response with respect to temperature –an initial period of gradual increase between 25°C and 32°C is followed by a period of sharp rise in steady state concentration between 32°C and 37°C, and subsequently a fast monotonic decrease when temperature exceeds 37°C.

CONCLUSION:  The observed rate of O2- production is proportional to the intracellular concentration of the fully-assembled activated membrane-bound enzyme NADPH oxidase (NOX). Based on our mathematical model, we speculate that between 25°C and 32°C, the assembly of NOX occurs in the transport limited regime, the rate of which increases weakly with temperature. For temperatures between 32°C and 37°C, the activation of NOX occurs in the kinetically controlled regime and thus increases rapidly with temperature. At temperatures above 37°C, the assembled NOX deactivates and/or internalizes rapidly, leading to a fast monotonic decrease of steady state O2-concentration with increasing temperature.

CLINICAL IMPLICATIONS:  Hypothermia has been advocated as a means to minimize ischemia reperfusion injury as might occur cerebro-vascular accidents and acute myocardial infarction. Our results indicate that hypothermia (as well as fever) could lead to a depression of immune cell function.

DISCLOSURE:  Victor Salloum, None.

Tuesday, November 1, 2005

10:30 AM - 12:00 PM


Figures

Tables

References

NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543