Yh. Zhang et al., IN-VIVO PRODUCTION OF HEAT-SHOCK PROTEIN IN MOUSE PERITONEAL-MACROPHAGES BY ADMINISTRATION OF LIPOPOLYSACCHARIDE, Infection and immunity, 62(10), 1994, pp. 4140-4144
The in vivo production of heat shock protein was studied by administra
tion of bacterial lipopolysaccharide (LPS) into mice. Heat shock prote
in 70 was detected in the extract of adherent peritoneal cells from mi
ce injected intraperitoneally with LPS by using the immunoblotting met
hod. The expression of heat shock protein 70 was found 2 days after in
jection of LPS and reached its peak 4 days after injection. The intrap
eritoneal injection of LPS induced the expression of heat shock protei
n 70, whereas its subcutaneous injection did not. The in vivo producti
on of heat shock protein 70 was inhibited by administration of LPS tog
ether with quercetin, an inhibitor of accumulation of heat shock prote
in 70 mRNA. Tumor necrosis factor alpha enhanced LPS-induced heat shoc
k protein production in vivo There was a decrease of gamma delta T cel
ls in the peritoneal cavity of mice injected intraperitoneally with LP
S. It was suggested that bacterial LPS is a stressful agent which indu
ces the in vivo heat shock protein response, and its administration le
ads to the production of heat shock protein 70 in peritoneal macrophag
es.