Zinc transporter SLC39A7 relieves zinc deficiency to suppress alternative macrophage activation and impairment of phagocytosis

Autor: Liangfei Niu, Ka-Wing Wong, Qinghua Xue, Wenyan Xie
Jazyk: angličtina
Rok vydání: 2020
Předmět:
0301 basic medicine
Pulmonology
Physiology
Immune Receptors
Biochemistry
White Blood Cells
Mathematical and Statistical Techniques
0302 clinical medicine
Animal Cells
Immune Physiology
Medicine and Health Sciences
Macrophage
Toll-like Receptors
Cation Transport Proteins
Innate Immune System
Gene knockdown
Immune System Proteins
Multidisciplinary
biology
Chemistry
Statistics
Nutritional Deficiencies
Cell Differentiation
Cell biology
Zinc
Cell Processes
Micronutrient Deficiencies
Physical Sciences
Cytokines
Medicine
Tumor necrosis factor alpha
Cellular Types
Research Article
Signal Transduction
Immune Cells
Phagocytosis
Science
Immunology
Research and Analysis Methods
Cell Line
Proinflammatory cytokine
03 medical and health sciences
medicine
Humans
Statistical Methods
Nutrition
Analysis of Variance
Blood Cells
Macrophages
Biology and Life Sciences
Proteins
Cell Biology
Molecular Development
Macrophage Activation
medicine.disease
Asthma
Solute carrier family
030104 developmental biology
Immune System
Zinc deficiency
biology.protein
SLC39A7
Mathematics
Developmental Biology
030215 immunology
Zdroj: PLoS ONE, Vol 15, Iss 7, p e0235776 (2020)
PLoS ONE
ISSN: 1932-6203
Popis: Macrophages are key phagocytic cells and play an important role in eliminating external microorganisms and endogenous danger signals. Dysregulation in macrophage functions have been reported in patients with asthma. Zinc homeostasis is critical in maintaining macrophage functions. The solute carrier (SLC) protein SLC39A7, a Zn2+ importer, has recently been linked to asthma. However, the roles of SLC39A7 in macrophage phagocytosis are not well understood. Here we found that phagocytosis efficiency was significantly decreased in SLC39A7-knockdown THP-1 cells, however the phagocytosis capability could be reversed with zinc supplementation. SLC39A7 deficiency skewed macrophages towards alternative activation, as indicated by increased expression of M2 activation marker CD206 and decreased expression of M1 activation marker NOS2. Consistent to this result, SLC39A7-knockdown cells produced reduced amounts of proinflammatory cytokines TNF- and IL-6. Furthermore, the mRNA level of receptor Clec4e previously known to be involved in phagocytosis of BCG was significantly reduced in SLC39A7 knockdown cells. Importantly, all these defects due to SLC39A7 deficiency could be reversed by zinc supplementation. Thus, zinc transporter SLC39A7 provide support for phagocytosis and classical macrophage activation.
Databáze: OpenAIRE
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