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

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 (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.


Total and free thiol β2GPI levels in mice following LPS injection.LPS decreased the (A) total but increased (B) free thiol β2GPI levels at 6 hrs after injection of LPS 1 μg/g body weight compared to injection of pyrogen free saline. n = 9 **p < 0.01. Unpaired two tailed Students t-test.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC5037396&req=5

f4: Total and free thiol β2GPI levels in mice following LPS injection.LPS decreased the (A) total but increased (B) free thiol β2GPI levels at 6 hrs after injection of LPS 1 μg/g body weight compared to injection of pyrogen free saline. n = 9 **p < 0.01. Unpaired two tailed Students t-test.

Mentions: Total β2GPI levels were significantly decreased in WT mice at 6 h after LPS injection compared to WT mice injected with pyrogen free saline, (86.1 ± 8.5 vs. 101 ± 10.28 mean (μg/ml) ± SD, n = 9, p = 0.004) (Fig. 4A). In contrast. the percentage of serum β2GPI in the free thiol form significantly increased after LPS injection compared to mice injected with pyrogen free saline, 108.4 ± 13.18 vs. 83.5 ± 16.94, mean (% of pooled normal standard) ± SD, n = 9, p = 0.003) (Fig. 4B). As expected there was no detectable β2GPI or free thiol β2GPI in the serum of β2GPI deficient mice (data not shown).


Gram Negative Bacterial Inflammation Ameliorated by the Plasma Protein Beta 2-Glycoprotein I
Total and free thiol β2GPI levels in mice following LPS injection.LPS decreased the (A) total but increased (B) free thiol β2GPI levels at 6 hrs after injection of LPS 1 μg/g body weight compared to injection of pyrogen free saline. n = 9 **p < 0.01. Unpaired two tailed Students t-test.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f4: Total and free thiol β2GPI levels in mice following LPS injection.LPS decreased the (A) total but increased (B) free thiol β2GPI levels at 6 hrs after injection of LPS 1 μg/g body weight compared to injection of pyrogen free saline. n = 9 **p < 0.01. Unpaired two tailed Students t-test.
Mentions: Total β2GPI levels were significantly decreased in WT mice at 6 h after LPS injection compared to WT mice injected with pyrogen free saline, (86.1 ± 8.5 vs. 101 ± 10.28 mean (μg/ml) ± SD, n = 9, p = 0.004) (Fig. 4A). In contrast. the percentage of serum β2GPI in the free thiol form significantly increased after LPS injection compared to mice injected with pyrogen free saline, 108.4 ± 13.18 vs. 83.5 ± 16.94, mean (% of pooled normal standard) ± SD, n = 9, p = 0.003) (Fig. 4B). As expected there was no detectable β2GPI or free thiol β2GPI in the serum of β2GPI deficient mice (data not shown).

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.