Y. Koh et al., Effects of heat pretreatment on histopathology, cytokine production, and surfactant in endotoxin-induced acute lung injury, INFLAMMATIO, 25(3), 2001, pp. 187-196
To determine the effect of heat stress on histopathology of acute lung inju
ry (ALI) caused by administration of lipopolysaccharide (LPS), and to deter
mine the roles of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 bet
a, interferon (IFN)-gamma IL-10 and surfactants in heat-induced tolerance t
o ALI, we administered either saline or LPS (3 mg/kg of body weight) intrav
enously to male Sprague-Dawley rats without and with heat pretreatment. Fiv
e hours after LPS or saline treatment (23 h after heat-pretreatment), sampl
es were obtained. We found that the histopathologic features of LPS-induced
ALI were attenuated by heat-pretreatment. Heat-pretreatment did not decrea
se the elevated plasma or BAL fluid levels of TNF-alpha, IL-1 beta, and IFN
-gamma by LPS. The plasma level of IL-10 in LPS-treated rats with heat-pret
reatment, however, was increased compared to that of LPS-treated rats witho
ut heat-pretreatment (P = 0.001). There were no differences in the BAL flui
d concentrations of light or heavy density pulmonary surfactant phospholipi
ds depending on heat-pretreatment in LPS-treated rats. These observations s
uggest that IL-10 might play a role in decreasing LPS-induced acute lung in
jury after heat-pretreatment.