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Медицинская библиотека · The Israel Medical Association journal : IMAJ · 2017

Increased CD11b+ cells and Interleukin-1 (IL-1) alpha levels during cardiomyopathy induced by chronic adrenergic activation.

Ben-Shoshan Jeremy, Jubran Ayman, Levy Ran, Keren Gad, Entin-Meer Michal

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Аннотация

BACKGROUND

Systemic CD11b+ cells have been associated with several cardiac diseases, such as chronic heart failure.

OBJECTIVES

To assess the levels of circulating CD11b+ cells and pro-inflammatory cytokines in cardiomyopathy induced by chronic adrenergic stimulation.

METHODS

Male Lewis rats were injected with low doses of isoproterenol (isoprel) for 3 months. Cardiac parameters were tested by echocardiography. The percentage of CD11b+ cells was tested by flow cytometry. The levels of inflammatory cytokines in the sera were determined by an inflammation array, and the expression levels of cardiac interleukin-1 (IL-1) receptors were analyzed by real-time polymerase chain reactions. Cardiac fibrosis and inflammation were determined by histological analysis.

RESULTS

Chronic isoprel administration resulted in increased heart rate, cardiac hypertrophy, elevated cardiac peri-vascular fibrosis, reduced fractional shortening, and increased heart weight per body weight ratio compared to control animals. This clinical presentation was associated with accumulation of CD11b+ cells in the spleen with no concomitant cardiac inflammation. Cardiac dysfunction was also associated with elevated sera levels of IL-1 alpha and over expression of cardiac IL-1 receptor type 2.

CONCLUSIONS

CD11b+ systemic levels and IL-1 signaling are associated with cardiomyopathy induced by chronic adrenergic stimulation. Further studies are needed to define the role of systemic immunomodulation in this cardiomyopathy.

Для цитирования: Ben-Shoshan Jeremy, Jubran Ayman, Levy Ran, Keren Gad, Entin-Meer Michal. Increased CD11b+ cells and Interleukin-1 (IL-1) alpha levels during cardiomyopathy induced by chronic adrenergic activation.. The Israel Medical Association journal : IMAJ. 2017.

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