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Interleukin 10 knockout frail mice develop cardiac and vascular dysfunction with increased age
Gautam Sikka1, Karen L Miller, Jochen Steppan
1Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland, USA. gsikka1@johnshopkins.edu
Experimental Gerontology
|November 20, 2012
Summary
Interleukin 10 (IL-10) deficiency in mice leads to vascular dysfunction and frailty. This study reveals that lack of IL-10 increases vascular stiffness and impairs relaxation, mimicking age-related cardiovascular decline.
Area of Science:
- Immunology
- Cardiovascular Biology
- Gerontology
Background:
- Cardiovascular dysfunction is a major cause of age-related mortality.
- Frailty is linked to inflammation and fatigue, common in aging.
- Interleukin 10 (IL-10) is an anti-inflammatory cytokine; its absence in mice causes a frailty-like phenotype.
Purpose of the Study:
- To investigate the role of IL-10 in maintaining vascular function.
- To elucidate the mechanisms behind IL-10's impact on vascular health during aging.
Main Methods:
- Ex-vivo force tension myography assessed vasorelaxation in IL-10 knockout (IL-10(tm/tm)) and control mice.
- Ultrasound measured pulse wave velocity (PWV) for vascular stiffness.
- Echocardiography evaluated cardiac structure and function.
Main Results:
- IL-10(tm/tm) mice exhibited higher mean arterial pressure and increased PWV, indicating stiffer vasculature.
- Impaired vasodilation and dose-dependent vasoconstriction were observed in IL-10(tm/tm) aortic rings.
- Aged IL-10(tm/tm) mice showed significant differences in cardiac size and function compared to controls.
Conclusions:
- Aging IL-10(tm/tm) mice develop stiffer vessels and reduced vascular relaxation due to increased COX-2 activity.
- These mice also present with cardiac enlargement and impaired function, suggesting a link between IL-10 and cardiovascular aging.
- The IL-10(tm/tm) mouse model effectively replicates the cardiovascular phenotype observed in frail, elderly individuals.
