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Article ; Online: T-bet

Khan, Saad / Winer, Daniel A

2022 Volume 43, Issue 11, Page(s) 855–857

Abstract: B cells are associated with the development of obesity-associated metabolic disease. Recently, Hägglöf, Vanz, et al. identified a novel obesity-related subset of B cells that are demarcated by the transcription factor T-bet and their pathogenic ability ... ...

Abstract	B cells are associated with the development of obesity-associated metabolic disease. Recently, Hägglöf, Vanz, et al. identified a novel obesity-related subset of B cells that are demarcated by the transcription factor T-bet and their pathogenic ability to worsen metabolic disease outcomes.
MeSH term(s)	Humans ; T-Box Domain Proteins/metabolism ; B-Lymphocytes/metabolism ; Obesity ; Metabolic Diseases/metabolism
Chemical Substances	T-Box Domain Proteins
Language	English
Publishing date	2022-10-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2022.09.011
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Article ; Online: Chronic inflammation and the hallmarks of aging.

Baechle, Jordan J / Chen, Nan / Makhijani, Priya / Winer, Shawn / Furman, David / Winer, Daniel A

Molecular metabolism

2023 Volume 74, Page(s) 101755

Abstract: Background: Recently, the hallmarks of aging were updated to include dysbiosis, disabled macroautophagy, and chronic inflammation. In particular, the low-grade chronic inflammation during aging, without overt infection, is defined as "inflammaging," ... ...

Abstract	Background: Recently, the hallmarks of aging were updated to include dysbiosis, disabled macroautophagy, and chronic inflammation. In particular, the low-grade chronic inflammation during aging, without overt infection, is defined as "inflammaging," which is associated with increased morbidity and mortality in the aging population. Emerging evidence suggests a bidirectional and cyclical relationship between chronic inflammation and the development of age-related conditions, such as cardiovascular diseases, neurodegeneration, cancer, and frailty. How the crosstalk between chronic inflammation and other hallmarks of aging underlies biological mechanisms of aging and age-related disease is thus of particular interest to the current geroscience research. Scope of review: This review integrates the cellular and molecular mechanisms of age-associated chronic inflammation with the other eleven hallmarks of aging. Extra discussion is dedicated to the hallmark of "altered nutrient sensing," given the scope of Molecular Metabolism. The deregulation of hallmark processes during aging disrupts the delicate balance between pro-inflammatory and anti-inflammatory signaling, leading to a persistent inflammatory state. The resultant chronic inflammation, in turn, further aggravates the dysfunction of each hallmark, thereby driving the progression of aging and age-related diseases. Main conclusions: The crosstalk between chronic inflammation and other hallmarks of aging results in a vicious cycle that exacerbates the decline in cellular functions and promotes aging. Understanding this complex interplay will provide new insights into the mechanisms of aging and the development of potential anti-aging interventions. Given their interconnectedness and ability to accentuate the primary elements of aging, drivers of chronic inflammation may be an ideal target with high translational potential to address the pathological conditions associated with aging.
MeSH term(s)	Humans ; Aged ; Inflammation ; Anti-Inflammatory Agents ; Cardiovascular Diseases
Chemical Substances	Anti-Inflammatory Agents
Language	English
Publishing date	2023-06-15
Publishing country	Germany
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2023.101755
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Article ; Online: The intestinal immune system and gut barrier function in obesity and ageing

Shemtov, Sarah J. / Emani, Rohini / Bielska, Olga / Covarrubias, Anthony J. / Verdin, Eric / Andersen, Julie K. / Winer, Daniel A.

The FEBS Journal. 2023 Sept., v. 290, no. 17 p.4163-4186

2023

Abstract: Obesity and ageing predispose to numerous, yet overlapping chronic diseases. For example, metabolic abnormalities, including insulin resistance (IR) and type 2 diabetes (T2D) are important causes of morbidity and mortality. Low‐grade chronic inflammation ...

Abstract	Obesity and ageing predispose to numerous, yet overlapping chronic diseases. For example, metabolic abnormalities, including insulin resistance (IR) and type 2 diabetes (T2D) are important causes of morbidity and mortality. Low‐grade chronic inflammation of tissues, such as the liver, visceral adipose tissue and neurological tissues, is considered a significant contributor to these chronic diseases. Thus, it is becoming increasingly important to understand what drives this inflammation in affected tissues. Recent evidence, especially in the context of obesity, suggests that the intestine plays an important role as the gatekeeper of inflammatory stimuli that ultimately fuels low‐grade chronic tissue inflammation. In addition to metabolic diseases, abnormalities in the intestinal mucosal barrier have been linked to a range of other chronic inflammatory conditions, such as neurodegeneration and ageing. The flow of inflammatory stimuli from the gut is in part controlled by local immunological inputs impacting the intestinal barrier. Here, we will review the impact of obesity and ageing on the intestinal immune system and its downstream consequences on gut barrier function, which is strongly implicated in the pathogenesis of obesity and age‐related diseases. In particular, we will discuss the effects of age‐related intestinal dysfunction on neurodegenerative diseases.
Keywords	absorption barrier ; adipose tissue ; immune system ; inflammation ; insulin resistance ; intestines ; liver ; mortality ; neurodegenerative diseases ; noninsulin-dependent diabetes mellitus ; obesity ; pathogenesis
Language	English
Dates of publication	2023-09
Size	p. 4163-4186.
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	REVIEW
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16558
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Article ; Online: Emerging concepts in intestinal immune control of obesity-related metabolic disease.

Khan, Saad / Luck, Helen / Winer, Shawn / Winer, Daniel A

Nature communications

2021 Volume 12, Issue 1, Page(s) 2598

Abstract: The intestinal immune system is an important modulator of glucose homeostasis and obesity-associated insulin resistance. Dietary factors, the intestinal microbiota and their metabolites shape intestinal immunity during obesity. The intestinal immune ... ...

Abstract	The intestinal immune system is an important modulator of glucose homeostasis and obesity-associated insulin resistance. Dietary factors, the intestinal microbiota and their metabolites shape intestinal immunity during obesity. The intestinal immune system in turn affects processes such as intestinal permeability, immune cell trafficking, and intestinal hormone availability, impacting systemic insulin resistance. Understanding these pathways might identify mechanisms underlying treatments for insulin resistance, such as metformin and bariatric surgery, or aid in developing new therapies and vaccination approaches. Here, we highlight evolving concepts centered on intestinal immunity, diet, and the microbiota to provide a working model of obesity-related metabolic disease.
MeSH term(s)	Animals ; B-Lymphocytes/immunology ; Cytokines/metabolism ; Diet Therapy ; Gastrointestinal Microbiome/immunology ; Humans ; Immune System/cytology ; Immune System/metabolism ; Inflammation/immunology ; Inflammation/metabolism ; Insulin Resistance/immunology ; Metabolic Diseases/immunology ; Metabolic Diseases/metabolism ; Metabolic Diseases/microbiology ; Metabolic Diseases/therapy ; Obesity/diet therapy ; Obesity/immunology ; Obesity/metabolism ; Obesity/therapy ; T-Lymphocytes/immunology
Chemical Substances	Cytokines
Language	English
Publishing date	2021-05-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-22727-7
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Article: Mechanosensing in macrophages and dendritic cells in steady-state and disease.

Lee, Megan / Du, Huixun / Winer, Daniel A / Clemente-Casares, Xavier / Tsai, Sue

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 1044729

Abstract: Macrophages and dendritic cells are myeloid cells that play critical roles in immune responses. Macrophages help to maintain homeostasis through tissue regeneration and the clearance of dead cells, but also mediate inflammatory processes against invading ...

Abstract	Macrophages and dendritic cells are myeloid cells that play critical roles in immune responses. Macrophages help to maintain homeostasis through tissue regeneration and the clearance of dead cells, but also mediate inflammatory processes against invading pathogens. As the most potent antigen-presenting cells, dendritic cells are important in connecting innate to adaptive immune responses
Language	English
Publishing date	2022-11-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.1044729
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Article: Regulation of the immune system by the insulin receptor in health and disease.

Makhijani, Priya / Basso, Paulo José / Chan, Yi Tao / Chen, Nan / Baechle, Jordan / Khan, Saad / Furman, David / Tsai, Sue / Winer, Daniel A

Frontiers in endocrinology

2023 Volume 14, Page(s) 1128622

Abstract: The signaling pathways downstream of the insulin receptor (InsR) are some of the most evolutionarily conserved pathways that regulate organism longevity and metabolism. InsR signaling is well characterized in metabolic tissues, such as liver, muscle, and ...

Abstract	The signaling pathways downstream of the insulin receptor (InsR) are some of the most evolutionarily conserved pathways that regulate organism longevity and metabolism. InsR signaling is well characterized in metabolic tissues, such as liver, muscle, and fat, actively orchestrating cellular processes, including growth, survival, and nutrient metabolism. However, cells of the immune system also express the InsR and downstream signaling machinery, and there is increasing appreciation for the involvement of InsR signaling in shaping the immune response. Here, we summarize current understanding of InsR signaling pathways in different immune cell subsets and their impact on cellular metabolism, differentiation, and effector versus regulatory function. We also discuss mechanistic links between altered InsR signaling and immune dysfunction in various disease settings and conditions, with a focus on age related conditions, such as type 2 diabetes, cancer and infection vulnerability.
MeSH term(s)	Humans ; Receptor, Insulin/metabolism ; Insulin/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Signal Transduction ; Immune System/metabolism
Chemical Substances	Receptor, Insulin (EC 2.7.10.1) ; Insulin
Language	English
Publishing date	2023-03-13
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1128622
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Article ; Online: Gut T Cells Feast on GLP-1 to Modulate Cardiometabolic Disease.

Tsai, Sue / Winer, Shawn / Winer, Daniel A

Cell metabolism

2019 Volume 29, Issue 4, Page(s) 787–789

Abstract: Glucagon-like peptide-1 (GLP-1) is an enteroendocrine hormone that controls insulin secretion, intestinal function, and food intake. Recently in Nature, He et al. (2019) reported that gut intraepithelial T cells regulate GLP-1 bioavailability by ... ...

Abstract	Glucagon-like peptide-1 (GLP-1) is an enteroendocrine hormone that controls insulin secretion, intestinal function, and food intake. Recently in Nature, He et al. (2019) reported that gut intraepithelial T cells regulate GLP-1 bioavailability by capturing it on GLP-1 receptors and impacting L-cell numbers. This study delineates a novel endocrine-immune axis through which intestinal immune cells regulate whole-body metabolism.
MeSH term(s)	Cardiovascular Diseases ; Enteroendocrine Cells ; Glucagon-Like Peptide 1 ; Humans ; Intestines ; Intraepithelial Lymphocytes ; Male
Chemical Substances	Glucagon-Like Peptide 1 (89750-14-1)
Language	English
Publishing date	2019-04-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2019.03.002
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Article ; Online: Adipose Tissue B Cells Come of Age: The AABs of Fat Inflammation.

Khan, Saad / Tsai, Sue / Winer, Daniel A

Cell metabolism

2019 Volume 30, Issue 6, Page(s) 997–999

Abstract: For nearly a decade, B cells residing locally within the adipose tissue have been linked to the control of metabolic homeostasis. In this issue, Camell et al. (2019) report an expansion of a unique age-associated B cell population in the visceral adipose ...

Abstract	For nearly a decade, B cells residing locally within the adipose tissue have been linked to the control of metabolic homeostasis. In this issue, Camell et al. (2019) report an expansion of a unique age-associated B cell population in the visceral adipose tissue that regulates insulin resistance and adipose dysfunction during aging.
MeSH term(s)	Adipose Tissue ; Aging ; B-Lymphocytes ; Homeostasis ; Humans ; Inflammasomes ; Inflammation ; Insulin Resistance ; NLR Family, Pyrin Domain-Containing 3 Protein
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP3 protein, human
Language	English
Publishing date	2019-12-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2019.11.007
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Article ; Online: Cholesterol accumulation impairs HIF-1α-dependent immunometabolic reprogramming of LPS-stimulated macrophages by upregulating the NRF2 pathway.

Ting, Kenneth K Y / Yu, Pei / Dow, Riley / Ibrahim, Hisham / Karim, Saraf / Polenz, Chanele K / Winer, Daniel A / Woo, Minna / Jongstra-Bilen, Jenny / Cybulsky, Myron I

Scientific reports

2024 Volume 14, Issue 1, Page(s) 11162

Abstract: Lipid accumulation in macrophages (Mφs) is a hallmark of atherosclerosis. Yet, how lipid loading modulates Mφ inflammatory responses remains unclear. We endeavored to gain mechanistic insights into how pre-loading with free cholesterol modulates Mφ ... ...

Abstract	Lipid accumulation in macrophages (Mφs) is a hallmark of atherosclerosis. Yet, how lipid loading modulates Mφ inflammatory responses remains unclear. We endeavored to gain mechanistic insights into how pre-loading with free cholesterol modulates Mφ metabolism upon LPS-induced TLR4 signaling. We found that activities of prolyl hydroxylases (PHDs) and factor inhibiting HIF (FIH) are higher in cholesterol loaded Mφs post-LPS stimulation, resulting in impaired HIF-1α stability, transactivation capacity and glycolysis. In RAW264.7 cells expressing mutated HIF-1α proteins resistant to PHDs and FIH activities, cholesterol loading failed to suppress HIF-1α function. Cholesterol accumulation induced oxidative stress that enhanced NRF2 protein stability and triggered a NRF2-mediated antioxidative response prior to and in conjunction with LPS stimulation. LPS stimulation increased NRF2 mRNA and protein expression, but it did not enhance NRF2 protein stability further. NRF2 deficiency in Mφs alleviated the inhibitory effects of cholesterol loading on HIF-1α function. Mutated KEAP1 proteins defective in redox sensing expressed in RAW264.7 cells partially reversed the effects of cholesterol loading on NRF2 activation. Collectively, we showed that cholesterol accumulation in Mφs induces oxidative stress and NRF2 stabilization, which when combined with LPS-induced NRF2 expression leads to enhanced NRF2-mediated transcription that ultimately impairs HIF-1α-dependent glycolytic and inflammatory responses.
MeSH term(s)	NF-E2-Related Factor 2/metabolism ; NF-E2-Related Factor 2/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Animals ; Lipopolysaccharides ; Mice ; Macrophages/metabolism ; Macrophages/drug effects ; Macrophages/immunology ; Cholesterol/metabolism ; RAW 264.7 Cells ; Signal Transduction/drug effects ; Oxidative Stress/drug effects ; Kelch-Like ECH-Associated Protein 1/metabolism ; Kelch-Like ECH-Associated Protein 1/genetics ; Up-Regulation/drug effects ; Toll-Like Receptor 4/metabolism
Language	English
Publishing date	2024-05-15
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-61493-6
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Article: The Immune Landscape of Visceral Adipose Tissue During Obesity and Aging.

Khan, Saad / Chan, Yi Tao / Revelo, Xavier S / Winer, Daniel A

Frontiers in endocrinology

2020 Volume 11, Page(s) 267

Abstract: Obesity and aging represent major health burdens to the global adult population. Both conditions promote the development of associated metabolic diseases such as insulin resistance. The visceral adipose tissue (VAT) is a site that becomes dysfunctional ... ...

Abstract	Obesity and aging represent major health burdens to the global adult population. Both conditions promote the development of associated metabolic diseases such as insulin resistance. The visceral adipose tissue (VAT) is a site that becomes dysfunctional during obesity and aging, and plays a significant role during their pathophysiology. The changes in obese and aging VAT are now recognized to be partly driven by a chronic local inflammatory state, characterized by immune cells that typically adopt an inflammatory phenotype during metabolic disease. Here, we summarize the current knowledge on the immune cell landscape of the VAT during lean, obese, and aged conditions, highlighting their similarities and differences. We also briefly discuss possible linked mechanisms that fuel obesity- and age-associated VAT dysfunction.
MeSH term(s)	Aging/immunology ; Aging/metabolism ; Aging/pathology ; Animals ; Humans ; Intra-Abdominal Fat/immunology ; Intra-Abdominal Fat/metabolism ; Obesity/immunology ; Obesity/metabolism ; Obesity/pathology
Language	English
Publishing date	2020-05-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2020.00267
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