title: Impaired phagocytosis of apoptotic cells causes accumulation of bone marrow-derived macrophages in aged mice.
abstract: Accumulation of tissue macrophages is a significant characteristic of disease-associated chronic inflammation, and facilitates the progression of disease pathology. However, the functional roles of these bone marrow-derived macrophages (BMDMs) in aging are unclear. Here, we identified agedependent macrophage accumulation in the bone marrow, showing that aging significantly increases the number of M1 macrophages and impairs polarization of BMDMs. We found that age-related dysregulation of BMDMs is associated with abnormal overexpression of the anti-inflammatory interleukin-10. BMDM dysregulation in aging impairs the expression levels of pro-inflammatory cytokines and genes involved in B-cell maturation and activation. Phagocytosis of apoptotic Jurkat cells by BMDMs was reduced because of low expression of phagocytic receptor CD14, indicating that increased apoptotic cells may result from defective phagocytosis of apoptotic cells in the BM of aged mice. Therefore, CD14 may represent a promising target for preventing BMDM dysregulation, and macrophage accumulation may provide diagnostic and therapeutic clues. [BMB Reports 2017; 50(1): 43-48].
authors.affiliation: Lee Gil Ya Cancer and Diabetes Institute, College of Medicine, Gachon University, Incheon 21999, Korea.
authors.forename: Ok-Hee
authors.initials: OH
authors.lastname: Kim
authors.affiliation: Lee Gil Ya Cancer and Diabetes Institute, College of Medicine, Gachon University, Incheon 21999, Korea.
authors.forename: Hyojung
authors.initials: H
authors.lastname: Kim
authors.affiliation: Lee Gil Ya Cancer and Diabetes Institute, College of Medicine, Gachon University, Incheon 21999, Korea.
authors.forename: Jinku
authors.initials: J
authors.lastname: Kang
authors.affiliation: Department of Physiology, College of Medicine, Gachon University, Incheon 21999, Korea.
authors.forename: Dongki
authors.initials: D
authors.lastname: Yang
authors.affiliation: Samsung Advanced Institute of Technology, Samsung Electronics Co. Ltd., Suwon 16678, Korea.
authors.forename: Yu-Hoi
authors.initials: YH
authors.lastname: Kang
authors.affiliation: Lee Gil Ya Cancer and Diabetes Institute, College of Medicine, Gachon University, Incheon 21999, Korea.
authors.forename: Dae Ho
authors.initials: DH
authors.lastname: Lee
authors.affiliation: Department of Nuclear Medicine, Seoul National University College of Medicine, Seoul 03080, Korea.
authors.forename: Gi Jeong
authors.initials: GJ
authors.lastname: Cheon
authors.affiliation: Well Aging Research Center, DGIST, Daegu 42988, Korea.
authors.forename: Sang Chul
authors.initials: SC
authors.lastname: Park
authors.affiliation: Lee Gil Ya Cancer and Diabetes Institute, College of Medicine; Department of Physiology, College of Medicine, Gachon University, Incheon 21999, Korea.
authors.forename: Byung-Chul
authors.initials: BC
authors.lastname: Oh
mesh_terms: D000375:Aging / Q000378:metabolism / Q000473:pathology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D017209:Apoptosis / Q000502:physiology*; D001854:Bone Marrow Cells / Q000166:cytology* / Q000378:metabolism; D002454:Cell Differentiation / Q000502:physiology; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000473:pathology; D016753:Interleukin-10 / Q000378:metabolism; D019169:Jurkat Cells; D018950:Lipopolysaccharide Receptors / Q000378:metabolism; D008264:Macrophages / Q000166:cytology* / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010587:Phagocytosis / Q000502:physiology*
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D018950:Lipopolysaccharide Receptors; D016753:Interleukin-10