1-palmitoyl-2-oleoylglycero-3-phosphoglycerol and Abscess

1-palmitoyl-2-oleoylglycero-3-phosphoglycerol has been researched along with Abscess* in 1 studies

Other Studies

1 other study(ies) available for 1-palmitoyl-2-oleoylglycero-3-phosphoglycerol and Abscess

ArticleYear
Treponemal phospholipids inhibit innate immune responses induced by pathogen-associated molecular patterns.
    The Journal of biological chemistry, 2003, Nov-07, Volume: 278, Issue:45

    Host innate immune responses to microbial components, known as pathogen-associated molecular patterns (PAMPs), are regulated and modified by cellular receptors and serum proteins, including Toll-like receptors (TLRs), CD14, and LPS-binding protein (LBP). We demonstrated that a treponemal membrane lipid inhibited PAMPs-induced immune responses. The chemical structure of the lipid was elucidated as a phosphatidylglycerol (PG) derivative, which is scarce in most mammalian tissues, but relatively abundant in treponemal membrane lipids. Natural and synthetic PG counterparts as well as related natural anionic phospholipids, phosphatidylinositol, phosphatidylserine, and cardiolipin, also demonstrated an inhibitory effect. Further, we noted that PG inhibited PAMPs-induced immune responses by blocking the binding of PAMPs with LBP and CD14. In addition, PG decreased proinflammatory cytokine production in serum of LPS-injected mice and depressed abscess formation in mice infected with treponemes. These results suggest that treponemal phospholipid interfere the function of LBP/CD14 and act as a modulator of innate immune responses.

    Topics: Abscess; Acute-Phase Proteins; Animals; Blotting, Western; Cardiolipins; Carrier Proteins; Cytokines; Female; Immunity; Interleukin-1; Interleukin-6; Lipopolysaccharide Receptors; Lipopolysaccharides; Luciferases; Membrane Glycoproteins; Membrane Lipids; Mice; Mice, Inbred BALB C; Mice, Inbred C3H; NF-kappa B; Phosphatidylglycerols; Phosphatidylinositols; Phosphatidylserines; Phospholipids; RNA, Messenger; Treponema; Treponemal Infections; Tumor Necrosis Factor-alpha

2003