Journal article
Aging results in accumulation of M1 and M2 hepatic macrophages and a differential response to gadolinium chloride
Histochemistry and cell biology, Vol.153(1), pp.37-48
11/06/2019
DOI: 10.1007/s00418-019-01827-y
PMID: 31691025
Abstract
Macrophages have vital roles in innate immunity by modulating the inflammatory response via their ability to alter their phenotype from pro-inflammatory (M1) to anti-inflammatory (M2). Aging increases activation of the innate immune system, and macrophage numbers increase in the aged liver. Since macrophages also produce free radical molecules, they are a potential source of age-related oxidative injury in the liver. This study evaluated macrophage phenotype in the aged liver and whether the increase in the number of macrophages with aging is associated with enhanced hepatic oxidative stress. Hepatic macrophage phenotype and oxidative stress were evaluated 2 days after a single intraperitoneal injection of saline or gadolinium chloride (GdCl
3
, 10 mg/kg) in young (6 months) and aged (24 months) Fischer 344 rats. GdCl
3
has been shown to decrease the expression of macrophage-specific markers and impair macrophage phagocytosis in the liver. Saline-treated aged rats demonstrated greater numbers of both M1 (HO-1
+
/iNOS
+
) and M2 (HO-1
+
/CD163
+
) macrophages, without evidence of a phenotypic shift. GdCl
3
did not alter levels of dihydroethidium fluorescence or malondialdehyde, suggesting that macrophages are not a major contributor to steady-state levels of oxidative stress. However, GdCl
3
decreased M1 and M2 macrophage markers in both age groups, an effect that was attenuated in aged rats. In old animals, GdCl
3
decreased iNOS expression to a greater extent than HO-1 or CD163. These results suggest a novel effect of aging on macrophage biology and that GdCl
3
shifts hepatic macrophage polarization to the M2 phenotype in aged animals.
Details
- Title: Subtitle
- Aging results in accumulation of M1 and M2 hepatic macrophages and a differential response to gadolinium chloride
- Creators
- Steven A Bloomer - Division of Science and Engineering, Penn State University, Abington CollegeEric D Moyer - Division of Science and Engineering, Penn State University, Abington CollegeKyle E Brown - Iowa City Veterans Administration Medical Center, Division of Gastroenterology-Hepatology, University of Iowa Roy J. and Lucille A. Carver College of Medicine, Program in Free Radical and Radiation Biology, University of Iowa Roy J. and Lucille A. Carver College of MedicineKevin C Kregel - Department of Health and Human Physiology, The University of Iowa
- Resource Type
- Journal article
- Publication Details
- Histochemistry and cell biology, Vol.153(1), pp.37-48
- Publisher
- Springer Berlin Heidelberg
- DOI
- 10.1007/s00418-019-01827-y
- PMID
- 31691025
- ISSN
- 0948-6143
- eISSN
- 1432-119X
- Grant note
- AG12350 / National Institute on Aging (http://dx.doi.org/10.13039/100000049)
- Language
- English
- Date published
- 11/06/2019
- Academic Unit
- Gastroenterology and Hepatology; Radiation Oncology; Provost Office Administration; Health and Human Physiology; Internal Medicine
- Record Identifier
- 9984213452102771
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