The effect of heat on cytokine production in rat endotoxemia

Abstract

Our study demonstrates that heat leads to pulmonary protection of short duration in severe endotoxemia. This protection was not mediated by plasma TNF-alpha, IL-10, or NO. Contrary to our hypothesis, pretreatment with heat increased rather than decreased the plasma MIP-2 concentration and alveolar macrophage production of MIP-2 in endotoxemia. The mechanism of heat-conferred pulmonary protection in endotoxemia remains unclear. Alveolar macrophages do not produce IL-10 in endotoxemia. The increased MIP-2 production by heated alveolar macrophages was not attributable to alterations in production of either TNF-alpha or IL-10. The significance of increased MIP-2 by endotoxin-exposed alveolar macrophages in heated rats is unknown.

Heat Stress Protects Against Lung Injury in the Neutropenic, Endotoxemic Rat

“…All other rats were placed in the oven at room temperature for 15 min. We have previously confirmed that HSP 70 inducible was present in the lung tissue and spleen of rats using this method (2).…”

“…Heat stress delivered prior to endotoxemia results in the production of heat shock proteins, which may play a protective role in cardiopulmonary dysfunction (1)(2)(3)(4)(5)(6). Heat shock proteins (HSP) are named based on their molecular weight.…”

The thermoregulatory consequences of heat stroke: Are cytokines involved?

“…The physiological relevance of 59.4 1C is questionable since this T a is not routinely encountered in nature (Adolph, 1947). Similarly, the majority of these studies exposed animals to pre-heated environmental chambers (Adolph, 1947;DuBose et al, 1983;Gathiram et al, 1987;Heidemann et al, 2000;Hubbard et al, 1977;Ohara et al, 1975;Wright, 1976;Wright et al, 1977), which represents a heat ''shock'' rather than heat ''stress'' paradigm . In vitro studies have also used heat shock paradigms (e.g., 42-43 1C water bath exposure for 1 h) to examine responses in different cell types (D'Souza et al, 1994;Watanabe et al, 1997Watanabe et al, , 1998.…”

Effect of Heat Shock Preconditioning on ROS Scavenging Activity in Rat Skeletal Muscle after Downhill Running

“…The ESR spectrum allows the original reactive radical to be identified and quantified. The spectrum of the reaction without muscle was recorded as a control, and a standard curve for SOD activity was constructed based on spectra with known SOD concentrations of 5,10,15,20,25,30,40, and 50 U/ml. The reaction mixture consisted of 50 μl of homogenate, 50 mM phosphoric acid buffer, 2 mM hypoxanthine (6-hydroxypurine), 0.4 U/ml xanthine oxidase, and 20 μl of 9.2 M 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) as a spin trap.…”

“…Recent papers have proposed that heat shock proteins (HSPs) can prevent exercise-induced muscle injury and play a role in skeletal muscle recovery and remodeling/adaptation processes after high-force eccentric exercise [7][8][9]. Heat shock preconditioning (HS) has been shown to reduce tissue injury induced by a variety of insults [10][11][12][13], and several investigations in rat skeletal muscle have demonstrated that HS protected muscle from disuse atrophy [14] and from oxidant damage during reloading after immobilization [15].…”