Abstract
The effects of dibutyryl cyclic AMP (DBcAMP) on the lethal toxicity of lipopolysaccharide (LPS) were investigated in mice made hypersensitive to LPS by administration with Corynebacterium parvum (C. parvum). The peritoneal macrophages in C. parvum-treated mice released a conspicuous level of TNFα in response to LPS in vitro. These macrophages exhibited much higher susceptibility to LPS-induced cytotoxicity than with resident or peptone-induced macrophages. Pretreatment of the C. parvum-induced macrophages with DBcAM significantly inhibited the TNFα production in response to LPS and decreased the susceptibility to LPS-induced cytotoxicity in vitro. Similar to the findings seen in in vitro experiments, in vivo administration with DBcAMP significantly inhibited the TNFα release in the sera of C. parvum-treated mice after LPS challenge and consequently decreased the susceptibility to LPS-induced shock. These results suggest that raising level of intracellular cAMP protects C. parvum-treated mice from hypersensitivity to lethal toxicity of LPS through downregulating TNFα synthesis.
| Original language | English |
|---|---|
| Pages (from-to) | 1-7 |
| Number of pages | 7 |
| Journal | Cellular Immunology |
| Volume | 162 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Apr 1995 |
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All Science Journal Classification (ASJC) codes
- Immunology
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Dibutyryl cyclic AMP protects Corynebacterium parvum-treated mice against lipopolysaccharide-induced lethal toxicity. / Inoue, Hidefumi; Takahashi, Shosuke; Nomoto, Kikuo; Yoshikai, Yasunobu.
In: Cellular Immunology, Vol. 162, No. 1, 04.1995, p. 1-7.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Dibutyryl cyclic AMP protects Corynebacterium parvum-treated mice against lipopolysaccharide-induced lethal toxicity
AU - Inoue, Hidefumi
AU - Takahashi, Shosuke
AU - Nomoto, Kikuo
AU - Yoshikai, Yasunobu
PY - 1995/4
Y1 - 1995/4
N2 - The effects of dibutyryl cyclic AMP (DBcAMP) on the lethal toxicity of lipopolysaccharide (LPS) were investigated in mice made hypersensitive to LPS by administration with Corynebacterium parvum (C. parvum). The peritoneal macrophages in C. parvum-treated mice released a conspicuous level of TNFα in response to LPS in vitro. These macrophages exhibited much higher susceptibility to LPS-induced cytotoxicity than with resident or peptone-induced macrophages. Pretreatment of the C. parvum-induced macrophages with DBcAM significantly inhibited the TNFα production in response to LPS and decreased the susceptibility to LPS-induced cytotoxicity in vitro. Similar to the findings seen in in vitro experiments, in vivo administration with DBcAMP significantly inhibited the TNFα release in the sera of C. parvum-treated mice after LPS challenge and consequently decreased the susceptibility to LPS-induced shock. These results suggest that raising level of intracellular cAMP protects C. parvum-treated mice from hypersensitivity to lethal toxicity of LPS through downregulating TNFα synthesis.
AB - The effects of dibutyryl cyclic AMP (DBcAMP) on the lethal toxicity of lipopolysaccharide (LPS) were investigated in mice made hypersensitive to LPS by administration with Corynebacterium parvum (C. parvum). The peritoneal macrophages in C. parvum-treated mice released a conspicuous level of TNFα in response to LPS in vitro. These macrophages exhibited much higher susceptibility to LPS-induced cytotoxicity than with resident or peptone-induced macrophages. Pretreatment of the C. parvum-induced macrophages with DBcAM significantly inhibited the TNFα production in response to LPS and decreased the susceptibility to LPS-induced cytotoxicity in vitro. Similar to the findings seen in in vitro experiments, in vivo administration with DBcAMP significantly inhibited the TNFα release in the sera of C. parvum-treated mice after LPS challenge and consequently decreased the susceptibility to LPS-induced shock. These results suggest that raising level of intracellular cAMP protects C. parvum-treated mice from hypersensitivity to lethal toxicity of LPS through downregulating TNFα synthesis.
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UR - http://www.scopus.com/inward/citedby.url?scp=0028923831&partnerID=8YFLogxK
U2 - 10.1006/cimm.1995.1044
DO - 10.1006/cimm.1995.1044
M3 - Article
C2 - 7704897
AN - SCOPUS:0028923831
VL - 162
SP - 1
EP - 7
JO - Cellular Immunology
JF - Cellular Immunology
SN - 0008-8749
IS - 1
ER -