DOI: 10.1128/iai.67.7.3399-3402.1999. Induction of Lethal Shock and Tolerance by<i>Porphyromonas gingivalis</i>Lipopolysaccharide in<scp>d</scp>-Galactosamine-Sensitized C3H/HeJ Mice

Induction of Lethal Shock and Tolerance byPorphyromonas gingivalisLipopolysaccharide ind-Galactosamine-Sensitized C3H/HeJ Mice

10.1128/iai.67.7.3399-3402.1999

Crossref journal-article

American Society for Microbiology

Infection and Immunity (235)

Abstract

ABSTRACTLipopolysaccharide (LPS) obtained fromPorphyromonas gingivaliswas found to exhibit marked lethal toxicity in galactosamine-sensitized C3H/HeJ mice. Although no lethality was observed in mice intraperitoneally challenged with 1 mg ofP. gingivalisLPS without galactosamine, when they were sensitized with 30 mg of galactosamine, challenge with 1 and 10 μg of LPS resulted in 67 and 100% lethality, respectively. The lethal dose of LPS was almost the same in LPS-responsive C57BL/6 mice and non-LPS-responsive C3H/HeJ mice. Furthermore, when 1 μg ofP. gingivalisLPS was administered to each mouse 90 min before the challenge with the same LPS with galactosamine, tolerance to the lethal action of LPS was induced, and the mice were completely protected from death, even at a dose 100-fold greater than the lethal dose of LPS. Neither a lethal effect nor induction of tolerance to the lethality ofP. gingivalisLPS was exhibited bySalmonellaLPS in galactosamine-sensitized C3H/HeJ mice. A protein-LPS complex derived fromPseudomonas aeruginosa, which exhibited strong lethality and induced tolerance to a subsequent challenge with a lethal dose of LPS in galactosamine-sensitized LPS-responsive mice, did not exhibit lethal toxicity in galactosamine-sensitized C3H/HeJ mice and failed to induce tolerance in these mice to the lethality ofP. gingivalisLPS. These results indicate thatP. gingivalisLPS plays the central role in the activation of non-LPS-responsive C3H/HeJ mice.

Authors 1

Ken-Ichi Tanamoto (first)

References 29 Referenced 9

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Rietschel E. T. Brade L. Schade U. Seydel U. Zäringer U. Kusumoto S. Brade H. Bacterial endotoxins: properties and structure of biologically active domains Surface structures of microorganisms and their interactions with the mammalian host. Schrinner E. Richmond M. H. Seibert G. Schwarz U. 1988 1 41 VCH Verlagsgesellschaft mbH Weinheim Federal Republic of Germany
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Tanamoto K. Azumi S. Haishima Y. Kumada H. Umemoto T. The lipid A moiety of Porphyromonas gingivalis LPS specifically mediates the activation of C3H/HeJ mice.J. Immunol.158199744304436 (10.4049/jimmunol.158.9.4430) / J. Immunol. / The lipid A moiety of Porphyromonas gingivalis LPS specifically mediates the activation of C3H/HeJ mice by Tanamoto K. (1997)
10.1515/znb-1952-0303
10.1038/26239

Dates

Type	When
Created	5 years, 7 months ago (Dec. 31, 2019, 10:36 a.m.)
Deposited	1 year, 11 months ago (Sept. 24, 2023, 10:39 a.m.)
Indexed	1 year, 10 months ago (Oct. 9, 2023, 2:45 p.m.)
Issued	26 years, 1 month ago (July 1, 1999)
Published	26 years, 1 month ago (July 1, 1999)
Published Print	26 years, 1 month ago (July 1, 1999)

Funders 0

None

BibTeX

@article{Tanamoto_1999, title={Induction of Lethal Shock and Tolerance byPorphyromonas gingivalisLipopolysaccharide in<scp>d</scp>-Galactosamine-Sensitized C3H/HeJ Mice}, volume={67}, ISSN={1098-5522}, url={http://dx.doi.org/10.1128/iai.67.7.3399-3402.1999}, DOI={10.1128/iai.67.7.3399-3402.1999}, number={7}, journal={Infection and Immunity}, publisher={American Society for Microbiology}, author={Tanamoto, Ken-Ichi}, editor={McGhee, J. R.}, year={1999}, month=jul, pages={3399–3402} }

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  "abstract": "<jats:title>ABSTRACT</jats:title><jats:p>Lipopolysaccharide (LPS) obtained from<jats:italic>Porphyromonas gingivalis</jats:italic>was found to exhibit marked lethal toxicity in galactosamine-sensitized C3H/HeJ mice. Although no lethality was observed in mice intraperitoneally challenged with 1 mg of<jats:italic>P. gingivalis</jats:italic>LPS without galactosamine, when they were sensitized with 30 mg of galactosamine, challenge with 1 and 10 \u03bcg of LPS resulted in 67 and 100% lethality, respectively. The lethal dose of LPS was almost the same in LPS-responsive C57BL/6 mice and non-LPS-responsive C3H/HeJ mice. Furthermore, when 1 \u03bcg of<jats:italic>P. gingivalis</jats:italic>LPS was administered to each mouse 90 min before the challenge with the same LPS with galactosamine, tolerance to the lethal action of LPS was induced, and the mice were completely protected from death, even at a dose 100-fold greater than the lethal dose of LPS. Neither a lethal effect nor induction of tolerance to the lethality of<jats:italic>P. gingivalis</jats:italic>LPS was exhibited by<jats:italic>Salmonella</jats:italic>LPS in galactosamine-sensitized C3H/HeJ mice. A protein-LPS complex derived from<jats:italic>Pseudomonas aeruginosa</jats:italic>, which exhibited strong lethality and induced tolerance to a subsequent challenge with a lethal dose of LPS in galactosamine-sensitized LPS-responsive mice, did not exhibit lethal toxicity in galactosamine-sensitized C3H/HeJ mice and failed to induce tolerance in these mice to the lethality of<jats:italic>P. gingivalis</jats:italic>LPS. These results indicate that<jats:italic>P. gingivalis</jats:italic>LPS plays the central role in the activation of non-LPS-responsive C3H/HeJ mice.</jats:p>",
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