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Published on: April 28, 2016
Ghrelin decreases microvascular leak during inflammation.
Rita O Kwan1, Elizabeth Cureton, Kristopher Dozier
1Department of Surgery, University of California, San Francisco-East Bay, Alameda County Medical Center, Oakland, California 94610, USA.
The Journal of Trauma
|January 14, 2010
Summary
Ghrelin reduces microvascular permeability during inflammation via the GHS-R1a receptor, independent of NF-kappaB. This finding is crucial for understanding inflammation in obese trauma patients.
Area of Science:
- Physiology
- Endocrinology
- Inflammation Research
Background:
- Obesity is linked to worse trauma outcomes, with lower ghrelin levels observed in obese individuals.
- Ghrelin's role in modulating microvascular permeability, especially during inflammation, remains to be fully elucidated.
Purpose of the Study:
- To investigate ghrelin's effect on microvascular permeability.
- To determine ghrelin's impact on microvascular permeability during lipopolysaccharide (LPS)-induced inflammation.
- To explore the involvement of the growth hormone secretagogue receptor (GHS-R1a) and nuclear factor kappa B (NF-kappaB) pathways.
Main Methods:
- Measurement of hydraulic permeability (Lp) in rat mesenteric postcapillary venules.
- Administration of ghrelin, LPS, a GHS-R1a receptor antagonist, and an NF-kappaB inhibitor.
- Comparative analysis of Lp under different treatment conditions.
Main Results:
- Ghrelin alone did not affect basal microvascular permeability.
- Ghrelin significantly decreased Lp during LPS-induced inflammation (1.60 +/- 0.16 vs. 2.27 +/- 0.14, p < 0.006).
- The GHS-R1a antagonist blunted ghrelin's effect by 86% (2.17 +/- 0.27 vs. 1.60 +/- 0.16, p < 0.018), while NF-kappaB inhibition had no significant effect.
Conclusions:
- Ghrelin exhibits a biphasic effect, decreasing microvascular permeability during LPS-induced inflammation via the GHS-R1a receptor.
- The anti-permeability effect of ghrelin during inflammation is independent of NF-kappaB signaling.
- Ghrelin may be a key mediator in inflammation, potentially contributing to adverse outcomes in obese trauma patients.
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