Role of innate immune cells in metabolism: from physiology to type 2 diabetes

2019 ◽  
Vol 41 (4) ◽  
pp. 531-545 ◽  
Author(s):  
Elise Dalmas
2021 ◽  
Vol 12 ◽  
Author(s):  
Alecia M. Blaszczak ◽  
Anahita Jalilvand ◽  
Willa A. Hsueh

The role of adipose tissue (AT) inflammation in obesity and its multiple related-complications is a rapidly expanding area of scientific interest. Within the last 30 years, the role of the adipocyte as an endocrine and immunologic cell has been progressively established. Like the macrophage, the adipocyte is capable of linking the innate and adaptive immune system through the secretion of adipokines and cytokines; exosome release of lipids, hormones, and microRNAs; and contact interaction with other immune cells. Key innate immune cells in AT include adipocytes, macrophages, neutrophils, and innate lymphoid cells type 2 (ILC2s). The role of the innate immune system in promoting adipose tissue inflammation in obesity will be highlighted in this review. T cells and B cells also play important roles in contributing to AT inflammation and are discussed in this series in the chapter on adaptive immunity.


2021 ◽  
pp. 1-27
Author(s):  
Zoi Michailidou ◽  
Mario Gomez-Salazar ◽  
Vasileia Ismini Alexaki

Metabolic disorders, such as obesity, type 2 diabetes mellitus, and nonalcoholic fatty liver disease, are characterized by chronic low-grade tissue and systemic inflammation. During obesity, the adipose tissue undergoes immunometabolic and functional transformation. Adipose tissue inflammation is driven by innate and adaptive immune cells and instigates insulin resistance. Here, we discuss the role of innate immune cells, that is, macrophages, neutrophils, eosinophils, natural killer cells, innate lymphoid type 2 cells, dendritic cells, and mast cells, in the adipose tissue in the healthy (lean) and diseased (obese) state and describe how their function is shaped by the obesogenic microenvironment, and humoral, paracrine, and cellular interactions. Moreover, we particularly outline the role of hypoxia as a central regulator in adipose tissue inflammation. Finally, we discuss the long-lasting effects of adipose tissue inflammation and its potential reversibility through drugs, caloric restriction, or exercise training.


2021 ◽  
Vol 22 (5) ◽  
pp. 2578
Author(s):  
Trim Lajqi ◽  
Christian Marx ◽  
Hannes Hudalla ◽  
Fabienne Haas ◽  
Silke Große ◽  
...  

Microglia, the innate immune cells of the CNS, exhibit long-term response changes indicative of innate immune memory (IIM). Our previous studies revealed IIM patterns of microglia with opposing immune phenotypes: trained immunity after a low dose and immune tolerance after a high dose challenge with pathogen-associated molecular patterns (PAMP). Compelling evidence shows that innate immune cells adopt features of IIM via immunometabolic control. However, immunometabolic reprogramming involved in the regulation of IIM in microglia has not been fully addressed. Here, we evaluated the impact of dose-dependent microglial priming with ultra-low (ULP, 1 fg/mL) and high (HP, 100 ng/mL) lipopolysaccharide (LPS) doses on immunometabolic rewiring. Furthermore, we addressed the role of PI3Kγ on immunometabolic control using naïve primary microglia derived from newborn wild-type mice, PI3Kγ-deficient mice and mice carrying a targeted mutation causing loss of lipid kinase activity. We found that ULP-induced IIM triggered an enhancement of oxygen consumption and ATP production. In contrast, HP was followed by suppressed oxygen consumption and glycolytic activity indicative of immune tolerance. PI3Kγ inhibited glycolysis due to modulation of cAMP-dependent pathways. However, no impact of specific PI3Kγ signaling on immunometabolic rewiring due to dose-dependent LPS priming was detected. In conclusion, immunometabolic reprogramming of microglia is involved in IIM in a dose-dependent manner via the glycolytic pathway, oxygen consumption and ATP production: ULP (ultra-low-dose priming) increases it, while HP reduces it.


Author(s):  
Rodolfo Perez-Alamino ◽  
Raquel Cuchacovich ◽  
Luis R. Espinoza ◽  
Constance P. Porretta ◽  
Arnold H. Zea

2019 ◽  
Vol 12 (2) ◽  
pp. 69-79
Author(s):  
Tajudeen Yahaya ◽  
Mutiu Sifau

Inadequate breastfeeding or its total neglect has been mentioned in several studies as a contributing factor to the globally rising incidence of Type 2 diabetes mellitus (T2DM). However, the anti-diabetic role of breast-milk has not been given much attention. As such, this study was initiated to review and bring to update on the role of breastfeeding in the risk reduction of T2DM. Relevant information on the topic was retrieved from the reliable science databases, including PubMed, MedLine, Google Scholar, Researchgate, etc. The results showed that breast-milk is not energy dense and contains several health-enhancing bioactive molecules, including adipokines, antimicrobial and growth factors, cytokines, nutrients, and immune cells. Adipokines interact with the central nervous system to modulate certain physiological processes involved in energy balance, thereby programming an infant to be at a reduced risk for overweight, obesity and T2DM later in life. The antimicrobial and growth factors, as well as immune cells and bioactive nutrients may stimulate the growth of beneficial bacteria and/or inhibit the growth of pathogens. Thus, strengthen neonate defense mechanisms to effectively prevent infections as well as short and long-term disorders such as obesity and T2DM. In conclusion, nursing mothers are advised to breastfeed babies adequately before introducing them to complementary foods. To cater to the need of babies who may not have access to breastfeeding, healthcare providers should formulate infant formula using breast-milk components as basic constituents.


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