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Abnormal lipopolysaccharide binding protein as marker of gastrointestinal inflammation in Parkinson disease.

Pal GD, Shaikh M, Forsyth CB, Ouyang B, Keshavarzian A, Shannon KM - Front Neurosci (2015)

Bottom Line: The LBP level between the PD and control groups was compared using analysis of covariance.In PD subjects, we did not find a correlation between mean LBP level and disease severity.However, there was significant variability in LBP levels within the PD and control groups, limiting its utility as a stand-alone biomarker.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurological Sciences, Rush University Medical Center Chicago, IL, USA.

ABSTRACT

Objective: An inflammation-driven model of PD has been proposed based on the endotoxin lipopolysaccaride (LPS), a potential source of inflammation in the gastrointestinal system linked to neurotoxicity. Systemic exposure to bacterial endotoxin (LPS) can be determined by measuring plasma LPS binding protein (LBP). We aimed to evaluate whether lipopolysaccharide binding protein (LBP) can be used to distinguish PD subjects from control subjects and to assess whether LBP levels correlate with PD disease severity.

Methods: We measured plasma LBP (ng/ml) using an ELISA kit in 94 PD subjects of various stages and 97 control subjects. Disease severity was assessed using the UPDRS and Hoehn and Yahr staging. The LBP level between the PD and control groups was compared using analysis of covariance. Spearman correlation was used to explore the relationship between LBP level and disease severity.

Results: The mean LBP level in PD subjects (n = 94) was significantly different from control subjects (n = 95, p = 0.018). In PD subjects, we did not find a correlation between mean LBP level and disease severity.

Conclusions: Our data suggests that LBP is one GI biomarker related to LPS induced neurotoxicity. However, there was significant variability in LBP levels within the PD and control groups, limiting its utility as a stand-alone biomarker. This study supports the role of LPS induced neurotoxicity in PD and further exploration of this pathway may be useful in developing sensitive and specific biomarkers for PD.

No MeSH data available.


Related in: MedlinePlus

LBP levels in PD and control subjects. Plasma LBP is significantly lower in PD patients. However, there remains significant overlap between the two groups and wide variability regarding the assay in both groups. Data are presented as means (ng/ml).
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Figure 1: LBP levels in PD and control subjects. Plasma LBP is significantly lower in PD patients. However, there remains significant overlap between the two groups and wide variability regarding the assay in both groups. Data are presented as means (ng/ml).

Mentions: To determine possible outliers, z-scores were obtained and values that were ≥3 standard deviations were removed. Four outliers were excluded in this fashion (all in the control group) and additional analyses were performed. There remained a significant difference in LBP levels between the PD group (n = 94, LBP 9344 ± 6694 ng/ml) and the control group (n = 95, 11280 ± 7422 ng/ml) (U = 3573.5, p = 0.018) (Figure 1). There was also a significant difference between GISSC scores and bowel movements per week in the PD group compared with the control group (Table 2).


Abnormal lipopolysaccharide binding protein as marker of gastrointestinal inflammation in Parkinson disease.

Pal GD, Shaikh M, Forsyth CB, Ouyang B, Keshavarzian A, Shannon KM - Front Neurosci (2015)

LBP levels in PD and control subjects. Plasma LBP is significantly lower in PD patients. However, there remains significant overlap between the two groups and wide variability regarding the assay in both groups. Data are presented as means (ng/ml).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4555963&req=5

Figure 1: LBP levels in PD and control subjects. Plasma LBP is significantly lower in PD patients. However, there remains significant overlap between the two groups and wide variability regarding the assay in both groups. Data are presented as means (ng/ml).
Mentions: To determine possible outliers, z-scores were obtained and values that were ≥3 standard deviations were removed. Four outliers were excluded in this fashion (all in the control group) and additional analyses were performed. There remained a significant difference in LBP levels between the PD group (n = 94, LBP 9344 ± 6694 ng/ml) and the control group (n = 95, 11280 ± 7422 ng/ml) (U = 3573.5, p = 0.018) (Figure 1). There was also a significant difference between GISSC scores and bowel movements per week in the PD group compared with the control group (Table 2).

Bottom Line: The LBP level between the PD and control groups was compared using analysis of covariance.In PD subjects, we did not find a correlation between mean LBP level and disease severity.However, there was significant variability in LBP levels within the PD and control groups, limiting its utility as a stand-alone biomarker.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurological Sciences, Rush University Medical Center Chicago, IL, USA.

ABSTRACT

Objective: An inflammation-driven model of PD has been proposed based on the endotoxin lipopolysaccaride (LPS), a potential source of inflammation in the gastrointestinal system linked to neurotoxicity. Systemic exposure to bacterial endotoxin (LPS) can be determined by measuring plasma LPS binding protein (LBP). We aimed to evaluate whether lipopolysaccharide binding protein (LBP) can be used to distinguish PD subjects from control subjects and to assess whether LBP levels correlate with PD disease severity.

Methods: We measured plasma LBP (ng/ml) using an ELISA kit in 94 PD subjects of various stages and 97 control subjects. Disease severity was assessed using the UPDRS and Hoehn and Yahr staging. The LBP level between the PD and control groups was compared using analysis of covariance. Spearman correlation was used to explore the relationship between LBP level and disease severity.

Results: The mean LBP level in PD subjects (n = 94) was significantly different from control subjects (n = 95, p = 0.018). In PD subjects, we did not find a correlation between mean LBP level and disease severity.

Conclusions: Our data suggests that LBP is one GI biomarker related to LPS induced neurotoxicity. However, there was significant variability in LBP levels within the PD and control groups, limiting its utility as a stand-alone biomarker. This study supports the role of LPS induced neurotoxicity in PD and further exploration of this pathway may be useful in developing sensitive and specific biomarkers for PD.

No MeSH data available.


Related in: MedlinePlus