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Rhodobacter azotoformans LPS (RAP99-LPS) Is a TLR4 Agonist That Inhibits Lung Metastasis and Enhances TLR3-Mediated Chemokine Expression

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Title: Rhodobacter azotoformans LPS (RAP99-LPS) Is a TLR4 Agonist That Inhibits Lung Metastasis and Enhances TLR3-Mediated Chemokine Expression
Authors: Murakami, Kaoru Browse this author
Kamimura, Daisuke Browse this author
Hasebe, Rie Browse this author
Uchida, Mona Browse this author
Abe, Nobuya Browse this author
Yamamoto, Reiji Browse this author
Jiang, Jing-Jing Browse this author
Hidaka, Yasuhiro Browse this author
Nakanishi, Yuko Browse this author
Fujita, Shuzo Browse this author
Toda, Yuki Browse this author
Toda, Nobuhiro Browse this author
Tanaka, Hiroki Browse this author
Akira, Shizuo Browse this author
Tanaka, Yuki Browse this author
Murakami, Masaaki Browse this author →KAKEN DB
Keywords: RAP99-LPS
Issue Date: 25-May-2021
Publisher: Frontiers Media
Journal Title: Frontiers in immunology
Volume: 12
Start Page: 675909
Publisher DOI: 10.3389/fimmu.2021.675909
Abstract: The lipopolysaccharides (LPSs) of Rhodobacter are reported to be TLR4 antagonists. Accordingly, the extract of Rhodobacter azotoformans (RAP99) is used as a health supplement for humans and animals in Japan to regulate immune responses in vivo. We previously analyzed the LPS structure of RAP99 (RAP99-LPS) and found it is different from that of E. coli-LPS but similar to lipid A from Rhodobacter sphaeroides (RSLA), a known antagonist of TLR4, with both having three C14 fatty acyl groups, two C10 fatty acyl groups, and two phosphates. Here we show that RAP99-LPS has an immune stimulatory activity and acts as a TLR4 agonist. Pretreatment of RAP99-LPS suppressed E. coli-LPS-mediated weight loss, suggesting it is an antagonist against E. coli-LPS like other LPS isolated from Rhodobacter. However, injections of RAP99-LPS caused splenomegaly and increased immune cell numbers in C57BL/6 mice but not in C3H/HeJ mice, suggesting that RAP99-LPS stimulates immune cells via TLR4. Consistently, RAP99-LPS suppressed the lung metastasis of B16F1 tumor cells and enhanced the expression of TLR3-mediated chemokines. These results suggest that RAP99-LPS is a TLR4 agonist that enhances the activation status of the immune system to promote anti-viral and anti-tumor activity in vivo.
Type: article
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

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