Porphyromonas gingivalisとは異なりEscherichia coli由来のリポ多糖の全身投与は新環境が誘発したマウスの移所行動の増大を抑制する

Lipopolysaccharide (LPS), a component of the Gram-negative bacterial cell wall, activates Toll-like receptors (TLRs). Porphyromonas gingivalis (Pg) appears to play a role in the development of periodontal disease. In vitro studies have suggested that unlike LPS derived from Escherichia coli (Ec-LPS)...

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Published in日本薬理学会年会要旨集 p. 4-B-O13-4
Main Authors 斉藤, 幸治, 泉福, 英信, 青野, 悠里, 三枝, 禎
Format Journal Article
LanguageJapanese
Published 公益社団法人 日本薬理学会 2022
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ISSN2435-4953
DOI10.1254/jpssuppl.96.0_4-B-O13-4

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Summary:Lipopolysaccharide (LPS), a component of the Gram-negative bacterial cell wall, activates Toll-like receptors (TLRs). Porphyromonas gingivalis (Pg) appears to play a role in the development of periodontal disease. In vitro studies have suggested that unlike LPS derived from Escherichia coli (Ec-LPS), which stimulates TLR4, LPS derived from Pg (Pg-LPS) may inhibit the TLR4. Mice exposed to a novel environment show hyperlocomotion that is inhibited by systemic administration of Ec-LPS. However, whether Pg-LPS influences novelty-induced locomotion is unknown. Therefore, we carried out an open field test to analyze the effects of Pg-LPS. For comparison, effects of Ec-LPS were also studied. Male ddY mouse (25-30 g) were used. The movement of each mouse in the open field was recorded for 30 min using a commercially available behavioural analysis system and the distance travelled (cm) was determined. Each compound was given intraperitoneally 4h before the open field test. Ec-LPS 500 and 840 µg/kg, but not 100 µg/kg, inhibited novelty-induced increases in distance travelled. Inhibition of hyperlocomotion by 840 µg/kg Ec-LPS was counteracted by co-administration of the TLR4 antagonist TAK-242 (3.0 mg/kg). Pg-LPS (100, 500 or 840 µg/kg) failed to alter novelty-induced locomotion. The present results provide in vivo evidence that Ec- and Pg-LPS induce different effects. Thus, Ec- but not Pg-LPS inhibits novelty-induced locomotor activity in mice by activating TLR4.
Bibliography:96_4-B-O13-4
ISSN:2435-4953
DOI:10.1254/jpssuppl.96.0_4-B-O13-4