Macrophage-mediated inflammation in metabolic disease

By A. Chawla, K. Nguyen, Y. Goh. Nature reviews. Immunology, 2011

1,303 citations recorded by the source corpus.

Metabolism and immunity are two fundamental systems of metazoans. The presence of immune cells, such as macrophages, in metabolic tissues suggests dynamic, ongoing crosstalk between these two regulatory systems. Here, we discuss how changes in the recruitment and activation of macrophages contribute to metabolic homeostasis. In particular, we focus our discussion on the pathogenic and protective functions of classically and alternatively activated macrophages, respectively, in experimental models of obesity and metabolic disease.

Subfields: Epidemiology, Immunology, Physiology

View Paper: https://www.semanticscholar.org/paper/a8d9bbd0d8c63c85294459c855cd7ba9a27c1fec

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Citations in the corpus

Adipose Tissue Remodeling: Its Role in Energy Metabolism and Metabolic Disorders (2016, background): “Moreover, iNKT cells can regulate the functions of regulatory T (Treg) cells via IL-2 production as well as those of M2 macrophages via IL-10 production in the adipose tissue (154).”
The Metabolic Signature of Macrophage Responses (2019, background): “In lean adipose tissue, M2 macrophages have a crucial role in maintaining the insulin sensitivity of adipocytes via the secretion of interleukin-10 (IL-10) (158, 167), a regulatory cytokine that potentiates insulin signaling in adipocytes (165).”
The role of estrogens in control of energy balance and glucose homeostasis. (2013, background): “Macrophages are elemental players in innate and adaptive immunity; over the past decade their roles in modulating whole-body metabolism and insulin sensitivity have been topics of increasing interest (295, 296).”
Tissue-specific signals control reversible program of localization and functional polarization of macrophages. (2014, positive): “Transcription factors, including STAT1, STAT6, C/EBPb, IRF-4, IRF5, and PPARg, have been shown to regulate transcription programs that control M1/M2 macrophage polarizations (Lawrence and Natoli, 2011).”
Tissue resident macrophages self-maintain locally throughout adult life with minimal contribution from circulating monocytes (2013, background): “, 2011), and metabolic disease (Chawla et al., 2011).”
Macrophage plasticity and polarization in tissue repair and remodelling (2013, background): “In this general context, IL-4-induced M2 polarized macrophages have recently been shown to regulate adaptive thermogenesis by producing catecholamines [46,47].”
Kupffer Cells in the Liver (2013, positive): “Much of our understanding of macrophage plasticity comes from resident macrophages in adipose tissue and nontissue macrophages (16, 132).”
Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes. (2014, background): “M1, which secrete pro-inflammatory cytokines such as IL-1b, IL-6, TNF-a, and the ‘‘alternatively activated macrophages’’ phenotype, termed M2 which produce anti-inflammatory cytokines such as IL-10 [4].”
Innate lymphoid type 2 cells sustain visceral adipose tissue eosinophils and alternatively activated macrophages (2013, background): “…in contrast, normal lean VAT contains eosinophils, alternatively activated mac rophages (AAM), invariant natural killer T cells (iNKTs), and regulatory T (T reg) cells that can promote insulin sensitivity and metabolic homeo stasis (Chawla et al., 2011; Schipper et al., 2012; Wu et al., 2011).”
Adipose Tissue Dysfunction as Determinant of Obesity-Associated Metabolic Complications (2019, background): “In obesity, alteration in adipose tissue remodeling may induce the dysregulation of adipose tissue secreted cytokines, leading to local and systemic inflammation and impaired adipogenesis of precursor cells, as further discussed later in this review [40,41].”