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Does high mobility group 1 protein function as a late mediator for LPS- or TNF-induced shock in galactosamine-sensitized mice?

Department of Biosciences, School of Science, Kitasato University, Sagamihara, Japan, hasunuma{at}jet.sci.kitasato-u.ac.jp

Hiroko Maruyama

Department of Pathology, School of Allied Health Sciences, Kitasato University, Sagamihara, Japan

Hiroaki Takimoto

Department of Biosciences, School of Science, Kitasato University, Sagamihara, Japan

Roland Ryll

Department of Biosciences, School of Science, Kitasato University, Sagamihara, Japan

Shigenori Tanaka

Seikagaku Corp., Tokyo, Japan

Yoshio Kumazawa

Department of Biosciences, School of Science, Kitasato University, Sagamihara, Japan

The role of high mobility group-1 protein (HMG-1) in LPS- and TNF-a-induced lethal shock in galactosamine (GalN)-sensitized mice was investigated. No detectable HMG-1 levels were observed by immunoblotting analysis in plasma from untreated or GalN-sensitized BALB/c mice 5 h after LPS injection, although significant levels of HMG-1 were detected in plasma 6 h after the challenge. All GalN-sensitized BALB/c but not BALB/lps^d mice succumbed by 6 h after LPS injection. When GalN-sensitized mice were injected with TNF-, the presence of HMG-1 was seen at 5.5 h in plasma of BALB/c mice and at 6 h in BALB/lps^d mice, although almost all GalN-sensitized BALB/c mice died by 6 h after challenge. The time-dependent phenomenon correlated with elevated serum aspartate aminotransferase (AST) levels and the appearance of apoptotic cells in livers. Administration of pooled plasma, equivalent to approximately 200 µg recombinant murine HMG-1, taken from mice on the verge of near death, did not result in induction of lethal shock in GalN-sensitized mice. Taken together with the late appearance of HMG-1 in moribund mice, these data suggest that HMG-1 does not decisively contribute to lethality in the GalN sensitization model.

Journal of Endotoxin Research, Vol. 8, No. 5, 391-398 (2002)
DOI: 10.1177/09680519020080050201


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