Emily Goldberg, PhD

Assistant Professsor

Physiology

Research Area

Persistent low-grade inflammation during aging underlies many chronic diseases, including insulin resistance, cardiovascular diseases, Alzheimer’s disease, and immunesenescence. Development of effective strategies to dampen age-related inflammation have been limited by our lack of understanding of the basic mechanisms that lead to its accumulation. We use integrative approaches to understand how immune-metabolic interactions regulate inflammation and can be harnessed to improve immunity and health during aging.

Publications

Nerve-associated macrophages control adipose homeostasis across lifespan and restrain age-related inflammation.

bioRxiv : the preprint server for biology

Gonzalez-Hurtado E, Leveau C, Li K, Qu R, Mishra M, Goldberg EL, Sidorov S, Yeung ST, Khairallah C, Gonzalez D, Shepard TM, Camell C, Artyomov MN, Kluger Y, Khanna KM, Dixit VD

A secondary β-hydroxybutyrate metabolic pathway linked to energy balance.

bioRxiv : the preprint server for biology

Moya-Garzon MD, Wang M, Li VL, Lyu X, Wei W, Tung AS, Raun SH, Zhao M, Coassolo L, Islam H, Oliveira B, Dai Y, Spaas J, Delgado-Gonzalez A, Donoso K, Alvarez-Buylla A, Franco-Montalban F, Letian A, Ward C, Liu L, Svensson KJ, Goldberg EL, Gardner CD, Little JP, Banik SM, Xu Y, Long JZ

Glucose restriction in antiviral defence.

Nature immunology

Goldberg EL

Ketone bodies as chemical signals for the immune system.

American journal of physiology. Cell physiology

Gonzatti MB, Goldberg E

Reversible histone deacetylase activity catalyzes lysine acylation.

bioRxiv : the preprint server for biology

Tsusaka T, Najar MA, Schwarz B, Bohrnsen E, Oses-Prieto JA, Lee C, Burlingame AL, Bosio CM, Burslem GM, Goldberg EL

Non-specific recognition of histone modifications by H3K9bhb antibody.

iScience

Tsusaka T, Oses-Prieto JA, Lee C, DeFelice BC, Burlingame AL, Goldberg EL

Non-specific recognition of histone modifications by H3K9bhb antibody.

bioRxiv : the preprint server for biology

Tsusaka T, Oses-Prieto JA, Lee C, DeFelice BC, Burlingame AL, Goldberg E

Innate immune cell-intrinsic ketogenesis is dispensable for organismal metabolism and age-related inflammation.

The Journal of biological chemistry

Goldberg EL, Letian A, Dlugos T, Leveau C, Dixit VD

Desmosterol suppresses macrophage inflammasome activation and protects against vascular inflammation and atherosclerosis.

Proceedings of the National Academy of Sciences of the United States of America

Zhang X, McDonald JG, Aryal B, Canfrán-Duque A, Goldberg EL, Araldi E, Ding W, Fan Y, Thompson BM, Singh AK, Li Q, Tellides G, Ordovás-Montanes J, García Milian R, Dixit VD, Ikonen E, Suárez Y, Fernández-Hernando C

IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2.

Cell metabolism

Goldberg EL, Shchukina I, Youm YH, Ryu S, Tsusaka T, Young KC, Camell CD, Dlugos T, Artyomov MN, Dixit VD

Integration of immune-metabolic signals to preserve healthy aging.

Translational medicine of aging

Goldberg EL

Investigating Ketone Bodies as Immunometabolic Countermeasures against Respiratory Viral Infections.

Med (New York, N.Y.)

Stubbs BJ, Koutnik AP, Goldberg EL, Upadhyay V, Turnbaugh PJ, Verdin E, Newman JC

How Inflammation Blunts Innate Immunity in Aging.

Interdisciplinary topics in gerontology and geriatrics

Goldberg EL, Shaw AC, Montgomery RR

Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue.

Nature metabolism

Goldberg EL, Shchukina I, Asher JL, Sidorov S, Artyomov MN, Dixit VD

Ketogenic diet activates protective γδ T cell responses against influenza virus infection.

Science immunology

Goldberg EL, Molony RD, Kudo E, Sidorov S, Kong Y, Dixit VD, Iwasaki A

Aging Induces an Nlrp3 Inflammasome-Dependent Expansion of Adipose B Cells That Impairs Metabolic Homeostasis.

Cell metabolism

Camell CD, Günther P, Lee A, Goldberg EL, Spadaro O, Youm YH, Bartke A, Hubbard GB, Ikeno Y, Ruddle NH, Schultze J, Dixit VD

Bone Marrow: An Immunometabolic Refuge during Energy Depletion.

Cell metabolism

Goldberg EL, Dixit VD

Anti-inflammatory effects of oestrogen mediate the sexual dimorphic response to lipid-induced insulin resistance.

The Journal of physiology

Camporez JP, Lyu K, Goldberg EL, Zhang D, Cline GW, Jurczak MJ, Dixit VD, Petersen KF, Shulman GI

Inflammasome-driven catecholamine catabolism in macrophages blunts lipolysis during ageing.

Nature

Camell CD, Sander J, Spadaro O, Lee A, Nguyen KY, Wing A, Goldberg EL, Youm YH, Brown CW, Elsworth J, Rodeheffer MS, Schultze JL, Dixit VD

β-Hydroxybutyrate Deactivates Neutrophil NLRP3 Inflammasome to Relieve Gout Flares.

Cell reports

Goldberg EL, Asher JL, Molony RD, Shaw AC, Zeiss CJ, Wang C, Morozova-Roche LA, Herzog RI, Iwasaki A, Dixit VD

Carnitine acetyltransferase (CRAT) expression in macrophages is dispensable for nutrient stress sensing and inflammation.

Molecular metabolism

Goldberg EL, Dixit VD

Immune memory-boosting dose of rapamycin impairs macrophage vesicle acidification and curtails glycolysis in effector CD8 cells, impairing defense against acute infections.

Journal of immunology (Baltimore, Md. : 1950)

Goldberg EL, Smithey MJ, Lutes LK, Uhrlaub JL, Nikolich-Žugich J

Acute neonatal infections 'lock-in' a suboptimal CD8+ T cell repertoire with impaired recall responses.

PLoS pathogens

Rudd BD, Venturi V, Smith NL, Nzingha K, Goldberg EL, Li G, Nikolich-Zugich J, Davenport MP

Contrasting effects of chronic, systemic treatment with mTOR inhibitors rapamycin and metformin on adult neural progenitors in mice.

Age (Dordrecht, Netherlands)

Kusne Y, Goldberg EL, Parker SS, Hapak SM, Maskaykina IY, Chew WM, Limesand KH, Brooks HL, Price TJ, Sanai N, Nikolich-Zugich J, Ghosh S

Publications

Nerve-associated macrophages control adipose homeostasis across lifespan and restrain age-related inflammation.

A secondary β-hydroxybutyrate metabolic pathway linked to energy balance.

Glucose restriction in antiviral defence.

Ketone bodies as chemical signals for the immune system.

Reversible histone deacetylase activity catalyzes lysine acylation.

Non-specific recognition of histone modifications by H3K9bhb antibody.

Non-specific recognition of histone modifications by H3K9bhb antibody.

Innate immune cell-intrinsic ketogenesis is dispensable for organismal metabolism and age-related inflammation.

Desmosterol suppresses macrophage inflammasome activation and protects against vascular inflammation and atherosclerosis.

IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2.

Integration of immune-metabolic signals to preserve healthy aging.

Investigating Ketone Bodies as Immunometabolic Countermeasures against Respiratory Viral Infections.

How Inflammation Blunts Innate Immunity in Aging.

Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue.

Ketogenic diet activates protective γδ T cell responses against influenza virus infection.

Aging Induces an Nlrp3 Inflammasome-Dependent Expansion of Adipose B Cells That Impairs Metabolic Homeostasis.

Bone Marrow: An Immunometabolic Refuge during Energy Depletion.

Anti-inflammatory effects of oestrogen mediate the sexual dimorphic response to lipid-induced insulin resistance.

Inflammasome-driven catecholamine catabolism in macrophages blunts lipolysis during ageing.

β-Hydroxybutyrate Deactivates Neutrophil NLRP3 Inflammasome to Relieve Gout Flares.

Carnitine acetyltransferase (CRAT) expression in macrophages is dispensable for nutrient stress sensing and inflammation.

Growth Hormone Receptor Deficiency Protects against Age-Related NLRP3 Inflammasome Activation and Immune Senescence.

Editorial: "Crowning" eosinophils in adipose tissue: does location matter?

Regulation of Nlrp3 inflammasome by dietary metabolites.

Drivers of age-related inflammation and strategies for healthspan extension.

The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease.

Lifespan-extending caloric restriction or mTOR inhibition impair adaptive immunity of old mice by distinct mechanisms.

Immune memory-boosting dose of rapamycin impairs macrophage vesicle acidification and curtails glycolysis in effector CD8 cells, impairing defense against acute infections.

Acute neonatal infections 'lock-in' a suboptimal CD8+ T cell repertoire with impaired recall responses.

Contrasting effects of chronic, systemic treatment with mTOR inhibitors rapamycin and metformin on adult neural progenitors in mice.