A5024258221- Adipokines, Inflammation, and Metabolic Diseases
- Adipose Tissue and Metabolism
- Immune Cell Function and Interaction
- Immune cells in cancer
- Cardiovascular Disease and Adiposity
- Atherosclerosis and Cardiovascular Diseases
- Muscle Physiology and Disorders
- Phagocytosis and Immune Regulation
- Lipid metabolism and disorders
- Natural Products and Biological Research
- Regulation of Appetite and Obesity
- Fatty Acid Research and Health
- interferon and immune responses
- Metabolism, Diabetes, and Cancer
- Diet and metabolism studies
- Obesity, Physical Activity, Diet
- Asthma and respiratory diseases
- Immune Response and Inflammation
- IL-33, ST2, and ILC Pathways
- Calpain Protease Function and Regulation
- Birth, Development, and Health
- Cancer, Hypoxia, and Metabolism
- COVID-19 Clinical Research Studies
- Pancreatic function and diabetes
- RNA Research and Splicing
University of Michigan
2015-2024
Michigan United
2011-2024
Ann Arbor Center for Independent Living
2014-2024
Michigan Medicine
2013-2023
VA Ann Arbor Healthcare System
2020-2023
Texas Tech University
2023
Center for Non-Communicable Diseases
2009-2021
Institute of Immunology
2015-2021
Association on Higher Education And Disability
2016
Pulmonary Associates
1997-2013
Adipose tissue macrophages (ATMs) infiltrate adipose during obesity and contribute to insulin resistance. We hypothesized that migrating upon high-fat feeding may differ from those reside there under normal diet conditions. To this end, we found a novel F4/80+CD11c+ population of ATMs in obese mice was not seen lean mice. expressed many genes characteristic M2 or “alternatively activated” macrophages, including Ym1, arginase 1, Il10. Diet-induced decreased expression these while increasing...
Although recent studies show that adipose tissue macrophages (ATMs) participate in the inflammatory changes obesity and contribute to insulin resistance, properties of these cells are not well understood. We hypothesized ATMs recruited during a high-fat diet have unique compared with resident ATMs. Using dye (PKH26) pulse label vivo, we purified white diet. Comparison gene expression using real-time RT-PCR cDNA microarrays showed overexpress genes important macrophage migration phagocytosis,...
To establish the mechanism of phenotypic switch adipose tissue macrophages (ATMs) from an alternatively activated (M2a) to a classically (M1) phenotype with obesity.ATMs lean and obese (high-fat diet-fed) C57Bl/6 mice were analyzed by combination flow cytometry, immunofluorescence, expression analysis for M2a M1 genes. Pulse labeling ATMs PKH26 assessed recruitment rate spatially distinct regions.Resident in express marker macrophage galactose N-acetyl-galactosamine specific lectin 1 (MGL1)...
Background— There is a strong link between urbanization and type 2 diabetes mellitus. Although multitude of mechanisms have been proposed, there are no studies evaluating the impact ambient air pollutants propensity to develop We hypothesized that exposure fine particulate matter (<2.5 μm; PM 2.5 ) exaggerates diet-induced insulin resistance, adipose inflammation, visceral adiposity. Methods Results— Male C57BL/6 mice were fed high-fat chow for 10 weeks randomly assigned concentrated or...
Inappropriate excess of the steroid hormone aldosterone, which is a mineralocorticoid receptor (MR) agonist, associated with increased inflammation and risk cardiovascular disease. MR antagonists are cardioprotective antiinflammatory in vivo, evidence suggests that they mediate these effects part by aldosterone-independent mechanisms. Here we have shown on myeloid cells necessary for efficient classical macrophage activation proinflammatory cytokines. Macrophages from mice lacking (referred...
Obesity leads to a proinflammatory state with immune responses that include infiltration of adipose tissue macrophages. These macrophages are believed alter insulin sensitivity in adipocytes, but the mechanisms underlie this effect have not been characterized. We explored interaction between and adipocytes context both indirect direct coculture. Macrophage-secreted factors blocked action via downregulation GLUT4 IRS-1, leading decrease Akt phosphorylation impaired insulin-stimulated...
Objective The relationship between adipose tissue fibrosis, adipocyte hypertrophy, and preadipocyte hyperplasia in the context of obesity correlation these tissue‐based phenomena with systemic metabolic disease are poorly defined. goal this study was to clarify human determine adipose‐tissue based diabetes. Methods Visceral subcutaneous tissues from humans collected during bariatric surgery were studied QRTPCR, immunohistochemistry, flow cytometry for expression collagens fibrosis‐related...
Background The development of insulin resistance (IR) in mouse models obesity and type 2 diabetes mellitus (DM) is characterized by progressive accumulation inflammatory macrophages subpopulations T cells the visceral adipose. Regulatory (Tregs) may play a critical role modulating tissue inflammation via their interactions with both adaptive innate immune mechanisms. We hypothesized that an imbalance Tregs determinant adipose investigated IR/obesity through coordinated studies mice humans....
Age-related adiposity has been linked to chronic inflammatory diseases in late life. To date, the studies on adipose tissue leukocytes and aging have not taken into account heterogeneity of macrophages (ATMs), nor they examined how age impacts other such as T cells fat. Therefore, we performed a detailed examination ATM subtypes young old mice using state art techniques. Our results demonstrate qualitative changes ATMs with that generate decrease resident type 2 (M2) ATMs. The profile fat...
The proinflammatory activation of leukocytes in adipose tissue contributes to metabolic disease. How crosstalk between immune cells initiates and sustains inflammation remains an unresolved question. We have examined the hypothesis that macrophages (ATMs) interact with regulate function T cells. Dietary obesity was shown activate proliferation effector memory CD4(+) tissue. Our studies further demonstrate ATMs are functional antigen-presenting promote interferon-γ-producing from lean obese...
Obesity is associated with an activated macrophage phenotype in multiple tissues that contributes to tissue inflammation and metabolic disease. To evaluate the mechanisms by which obesity potentiates myeloid activation, we evaluated hypothesis activates cell production from bone marrow progenitors potentiate inflammatory responses tissues. High fat diet-induced generated both quantitative increases as well a potentiation of macrophages derived these progenitors. In vivo, hematopoietic stem...
Obesity is characterized by adipose tissue (AT) macrophage (ATM) accumulation, which promotes AT inflammation and dysfunction. Toll-like receptor 4 (TLR4) deficiency attenuates in obesity but does not impede the accumulation of ATMs. The purpose current study was to determine whether TLR4 alters ATM polarization. TLR4(-/-) wild-type mice were fed a low-fat, high-monounsaturated fat (HF(MUFA)), or high-saturated (HF(SFA)) diet for 16 weeks. Further, we used bone marrow transplant model...
An adaptive immune response triggered by obesity is characterized the activation of adipose tissue CD4(+) T cells unclear mechanisms. We have examined whether interactions between macrophages (ATMs) and contribute to metainflammation. Intravital microscopy identifies dynamic antigen-dependent ATMs in visceral fat. Mice deficient major histocompatibility complex class II (MHC II) showed protection from diet-induced obesity. Deletion MHC expression led an tissue-specific decrease...
Dynamic changes of adipose tissue leukocytes, including macrophage (ATM) and dendritic cells (ATDCs), contribute to obesity-induced inflammation metabolic disease. However, clear discrimination between ATDC ATM in has limited progress the field immunometabolism. In this study, we use CD64 distinguish ATDC, investigated temporal functional these myeloid populations during obesity. Flow cytometry immunostaining demonstrated that definition as F4/80+CD11b+ overlaps with other leukocytes...
Obesity causes dramatic proinflammatory changes in the adipose tissue immune environment, but relatively little is known regarding how this inflammation responds to weight loss (WL). To understand mechanisms by which meta-inflammation resolves during WL, we examined leukocytes mice after withdrawal of a high-fat diet. After 8 weeks achieved similar weights and glucose tolerance values as age-matched lean controls showed abnormal insulin tolerance. Despite fat mass normalization, total CD11c+...