Journal of Endotoxin Research

 

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Journal of Endotoxin Research, Vol. 5, No. 1-2, 23-30 (1999)
DOI: 10.1177/09680519990050011601

Induction of hypersensitivity to endotoxin lethality in mice by treatment with trehalose 6,6'-dimycolate but not with 2,3,6,6'-tetraacyl trehalose 2'-sulfate

Kenji Watanabe

Department of Bacteriology, Osaka City University Medical School, Osaka, Japan, Department of Biosciences, School of Science, Kitasato University, Sagamihara, Japan

Ryoichi Hasunuma

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

Tomoko Horikoshi

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

Hironobu Yamana

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

Hiroko Maruyama

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

Nagatoshi Fujiwara

Department of Bacteriology, Osaka City University Medical School, Osaka, Japan

Yoshio Kumazawa

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

Ikuya Yano

Department of Bacteriology, Osaka City University Medical School, Osaka, Japan

The mechanism by which priming with trehalose 6,6'-dimycolate (TDM, cord factor) induced hypersensitivity to endotoxin lethality was investigated. C57BL/6 and BALB/c mice primed with TDM succumbed to endotoxin shock, but BALB/c IFN-{gamma} knock-out (IFN-{gamma} —/—) mice showed resistance to LPS lethality. The levels of serum IFN-{gamma} peaked on day 4 after priming with TDM and kept significant levels, indicating that IFN-{gamma} plays a critical role for inducing hypersensitivity to LPS lethality. After challenge with LPS, TDM-primed mice produced higher amounts of serum TNF{alpha} and soluble CD14. A sulfolipid (SL, 2,3,6,6'-tetraacyl trehalose 2'-sulfate) did not induce the hypersensitivity and, conversely, suppressed the activity of TDM when administered together. Administration of TDM induced infiltration of mononuclear cells in liver, and apoptosis of cells present in the liver sinus was observed after LPS challenge. These results suggest that the hypersensitivity to LPS lethality is due to overproduction of cytokines and other molecules.


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