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Gram Negative Bacterial Inflammation Ameliorated by the Plasma Protein Beta 2-Glycoprotein I

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ABSTRACT

Lipopolysaccharide (LPS) is a major component of the outer wall of gram negative bacteria. In high doses LPS contributes to the inflammation in gram negative sepsis, and in low doses contributes to the low grade inflammation characteristic of the metabolic syndrome. We wanted to assess the role of beta2-glycoprotein I (β2GPI) a highly conserved plasma protein and its different biochemical forms in a mouse model of LPS systemic inflammation. Normal and β2GPI deficient mice were administered LPS through their veins and assessed for a range of inflammation markers in their blood and liver. Different biochemical forms of β2GPI were measured in normal mice given either saline or LPS. We show that β2GPI has a significant role in inhibiting LPS induced inflammation. In this study we provide some evidence that β2GPI serves a protective role in a mouse model of LPS inflammation. This resolves the controversy of previous studies which used LPS and β2GPI in test tube based models of LPS induced activation of white cells. We also highlight the potential relevance of a newly discovered biochemical form of β2GPI in LPS mediated inflammation and we speculate that this form has a protective role against LPS induced pathology.

No MeSH data available.


Related in: MedlinePlus

β2GPI deficient mice have an increase in serum ALT following LPS administration.(□) = WT = Wild Type mice, (■) = β2GPI−/− = β2-glycoprotein I deficient mice. n = 8 *p < 0.05, S = Pyrogen Free Saline, L = LPS. Mann-Whitney test.
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f3: β2GPI deficient mice have an increase in serum ALT following LPS administration.(□) = WT = Wild Type mice, (■) = β2GPI−/− = β2-glycoprotein I deficient mice. n = 8 *p < 0.05, S = Pyrogen Free Saline, L = LPS. Mann-Whitney test.

Mentions: Serum ALT, a specific marker of liver damage, was significantly increased in β2GPI−/− mice following LPS injection compared to injection of β2GPI−/− mice with pyrogen free saline n = 8, p = 0.02 (Fig. 3). There was no significant difference seen in WT mice (Fig. 3).


Gram Negative Bacterial Inflammation Ameliorated by the Plasma Protein Beta 2-Glycoprotein I
β2GPI deficient mice have an increase in serum ALT following LPS administration.(□) = WT = Wild Type mice, (■) = β2GPI−/− = β2-glycoprotein I deficient mice. n = 8 *p < 0.05, S = Pyrogen Free Saline, L = LPS. Mann-Whitney test.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037396&req=5

f3: β2GPI deficient mice have an increase in serum ALT following LPS administration.(□) = WT = Wild Type mice, (■) = β2GPI−/− = β2-glycoprotein I deficient mice. n = 8 *p < 0.05, S = Pyrogen Free Saline, L = LPS. Mann-Whitney test.
Mentions: Serum ALT, a specific marker of liver damage, was significantly increased in β2GPI−/− mice following LPS injection compared to injection of β2GPI−/− mice with pyrogen free saline n = 8, p = 0.02 (Fig. 3). There was no significant difference seen in WT mice (Fig. 3).

View Article: PubMed Central - PubMed

ABSTRACT

Lipopolysaccharide (LPS) is a major component of the outer wall of gram negative bacteria. In high doses LPS contributes to the inflammation in gram negative sepsis, and in low doses contributes to the low grade inflammation characteristic of the metabolic syndrome. We wanted to assess the role of beta2-glycoprotein I (&beta;2GPI) a highly conserved plasma protein and its different biochemical forms in a mouse model of LPS systemic inflammation. Normal and &beta;2GPI deficient mice were administered LPS through their veins and assessed for a range of inflammation markers in their blood and liver. Different biochemical forms of &beta;2GPI were measured in normal mice given either saline or LPS. We show that &beta;2GPI has a significant role in inhibiting LPS induced inflammation. In this study we provide some evidence that &beta;2GPI serves a protective role in a mouse model of LPS inflammation. This resolves the controversy of previous studies which used LPS and &beta;2GPI in test tube based models of LPS induced activation of white cells. We also highlight the potential relevance of a newly discovered biochemical form of &beta;2GPI in LPS mediated inflammation and we speculate that this form has a protective role against LPS induced pathology.

No MeSH data available.


Related in: MedlinePlus