Immuno-metabolism and adipose tissue: The key role of hematopoietic stem cells

Cousin, Béatrice; Casteilla, Louis; Laharrague, Patrick; Luche, Élodie; Lorsignol, Anne; Cuminetti, Vincent; Paupert, Jenny

doi:10.1016/j.biochi.2015.06.012

Cited by 19 publications

(17 citation statements)

References 91 publications

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“…34,35 Additionally, it has recently been demonstrated that adipose tissue containing hematopoietic progenitors is able to reconstitute normal blood cell levels in irradiated mice. 35,36 In the present study, we did not determine whether leukocytosis was reduced by the effects of iron supplementation on bone marrow or adipose tissue, but iron excess induced in different ways has been shown to damage bone marrow stromal cells as well as other vital organs that support hematopoiesis through the generation of ROS. 37 Conversely, an increase of ROS in adipose tissue is not consistent with the local reduction in PAI-1 we observed.…”

Section: Discussionmentioning

confidence: 99%

Effects of iron supplementation in mice with hypoferremia induced by obesity

Gotardo

Caria

Oliveira

et al. 2016

Exp Biol Med (Maywood)

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Iron is an important micronutrient, but it can also act as a dangerous element by interfering with glucose homeostasis and inflammation, two features that are already disturbed in obese subjects. In this work, we study the effects of systemic iron supplementation on metabolic and inflammatory responses in mice with hypoferremia induced by obesity to better characterize whether iron worsens the parameters that are already altered after 24 weeks of a high-fat diet (HFD). Mice were maintained on a control diet or a HFD for 24 weeks and received iron-III polymaltose (50 mg/kg/every 2 days) during the last two weeks. Glucose homeostasis (basal glucose and insulin test tolerance) and systemic and visceral adipose tissue (VAT) inflammation were assessed. Iron levels were measured in serum. The Prussian blue reaction was used in isolated macrophages to detect iron deposition. Iron supplementation resulted in an increased number of VAT macrophages that were positive for Prussian blue staining as well as increased serum iron levels. Systemic hepcidin, leptin, resistin, and monocyte chemoattractant protein-1 (MCP-1) levels were not altered by iron supplementation. Local adipose tissue inflammation was also not made worse by iron supplementation because the levels of hepcidin, MCP-1, leptin, and interleukin (IL)-6 were not altered. In contrast, iron supplementation resulted in an increased production of IL-10 by adipose tissue and VAT macrophages. Leukocytosis and VAT plasminogen activator inhibitor-1 (PAI-1) level were reduced, but insulin resistance was not altered after iron supplementation. In conclusion, systemic iron supplementation in mice with hypoferremia induced by obesity did not worsen inflammatory marker or adipose tissue inflammation or the metabolic status established by obesity. Iron deposition was observed in adipose tissue, mainly in macrophages, suggesting that these cells have mechanisms that promote iron incorporation without increasing the production of inflammatory mediators.

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Section: Discussionmentioning

confidence: 99%

Effects of iron supplementation in mice with hypoferremia induced by obesity

Gotardo

Caria

Oliveira

et al. 2016

Exp Biol Med (Maywood)

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“…Adipose tissue sense a number of hormonal, metabolic, and/or inflammatory signals (Kim et al, 2014;Cousin et al, 2015), as well as neuronal signals (Chi et al, 2018) and infectious episodes (Casteilla et al, 2011). The main modulator of AT is the nutritional status.…”

Section: Adipose Tissue Senses and Sends Multiple Signalsmentioning

confidence: 99%

“…In addition to AT's involvement in metabolic homeostasis, this tissue also contains large numbers of both hematopoietic stem and precursor cells (HSPCs) and ASCs (Baglioni et al, 2009;Kim et al, 2014;Cousin et al, 2015). These cells confer AT with a high regenerative potential, which is currently being investigated for therapeutic purposes (Poglio et al, 2010;Casteilla et al, 2011;Luche et al, 2015).…”

Section: The Accumulation Of Hematopoietic Stem and Precursor Cells Amentioning

confidence: 99%

“…However, recent data suggest that this immunosuppressive profile may not be constitutive, and may depend on the pathophysiologic context (Wang et al, 2014). In contrast, data on HSPCs and the latter's regenerative potential are scarce (Cousin et al, 2015). However, Poglio et al (2010) demonstrated that AT is a reservoir of functional mast cell progenitors and these progenitors may renew innate immunity in AT but also support innate immunity in other organs (Poglio et al, 2012).…”

Section: The Accumulation Of Hematopoietic Stem and Precursor Cells Amentioning

confidence: 99%

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Specific Biological Features of Adipose Tissue, and Their Impact on HIV Persistence

et al. 2019

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Although white AT can contribute to anti-infectious immune responses, it can also be targeted and perturbed by pathogens. The AT's immune involvement is primarily due to strong pro-inflammatory responses (with both local and paracrine effects), and the large number of fat-resident macrophages. Adipocytes also exert direct antimicrobial responses. In recent years, it has been found that memory T cells accumulate in AT, where they provide efficient secondary responses against viral pathogens. These observations have prompted researchers to re-evaluate the links between obesity and susceptibility to infections. In contrast, AT serves as a reservoir for several persistence pathogens, such as human adenovirus Ad-36, Trypanosoma gondii, Mycobacterium tuberculosis, influenza A virus, and cytomegalovirus (CMV). The presence and persistence of bacterial DNA in AT has led to the concept of a tissuespecific microbiota. The unexpected coexistence of immune cells and pathogens within the specific AT environment is intriguing, and its impact on anti-infectious immune responses requires further evaluation. AT has been recently identified as a site of HIV persistence. In the context of HIV infection, AT is targeted by both the virus and the antiretroviral drugs. AT's intrinsic metabolic features, large overall mass, and wide distribution make it a major tissue reservoir, and one that may contribute to the pathophysiology of chronic HIV infections. Here, we review the immune, metabolic, viral, and pharmacological aspects that contribute to HIV persistence in AT. We also evaluate the respective impacts of both intrinsic and HIV-induced factors on AT's involvement as a viral reservoir. Lastly, we examine the potential consequences of HIV persistence on the metabolic and immune activities of AT.

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“…The second groundbreaking discovery in the field of immunometabolism came from Ferrante and Chen’s group, who reported simultaneously that adipose tissue of obese mice is infiltrated with macrophages that contribute to adipose tissue inflammation and IR (2, 3). Since these initial discoveries in immunometabolism, it has been shown that a large number of immune cells and pathways regulate metabolic homeostasis in obese animals (4–11). …”

Section: Introductionmentioning

confidence: 99%

Obesity: An Immunometabolic Perspective

Mahata

2016

Front. Endocrinol.

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Obesity, characterized by chronic activation of inflammatory pathways, is a critical factor contributing to insulin resistance (IR) and type 2 diabetes (T2D). Free fatty acids (FFAs) are increased in obesity and are implicated as proximate causes of IR and induction of inflammatory signaling in adipose, liver, muscle, and pancreas. Cells of the innate immune system produce cytokines, and other factors that affect insulin signaling and result in the development of IR. In the lean state, adipose tissue is populated by adipose tissue macrophage of the anti-inflammatory M2 type (ATM2) and natural killer (NK) cells; this maintains the insulin-sensitive phenotype because ATM2 cells secrete IL10. In contrast, obesity induces lipolysis and release of pro-inflammatory FFAs and factors, such as chemokine (C–C motif) ligand 2 (CCL2) and tumor necrosis factor alpha (TNF-α), which recruit blood monocytes in adipose tissue, where they are converted to macrophages of the highly pro-inflammatory M1-type (ATM1). Activated ATM1 produce large amounts of pro-inflammatory mediators such as TNF-α, interleukin-1β, IL-6, leukotriene B4, nitric oxide (NO), and resistin that work in a paracrine fashion and cause IR in adipose tissue. In the liver, both pro-inflammatory Kupffer cells (M1-KCs) and recruited hepatic macrophages (Ly6Chigh) contribute to decreased hepatic insulin sensitivity. The present mini-review will update the bidirectional interaction between the immune system and obesity-induced changes in metabolism in adipose tissue and liver and the metabolic consequences thereof.

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Immuno-metabolism and adipose tissue: The key role of hematopoietic stem cells

Cited by 19 publications

References 91 publications

Effects of iron supplementation in mice with hypoferremia induced by obesity

Effects of iron supplementation in mice with hypoferremia induced by obesity

Specific Biological Features of Adipose Tissue, and Their Impact on HIV Persistence

Obesity: An Immunometabolic Perspective

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