IGF1 Shapes Macrophage Activation in Response to Immunometabolic Challenge

Standard

IGF1 Shapes Macrophage Activation in Response to Immunometabolic Challenge. / Spadaro, Olga; Camell, Christina D; Bosurgi, Lidia; Nguyen, Kim Y; Youm, Yun-Hee; Rothlin, Carla V; Dixit, Vishwa Deep.

in: CELL REP, Jahrgang 19, Nr. 2, 11.04.2017, S. 225-234.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Spadaro, O, Camell, CD, Bosurgi, L, Nguyen, KY, Youm, Y-H, Rothlin, CV & Dixit, VD 2017, 'IGF1 Shapes Macrophage Activation in Response to Immunometabolic Challenge', CELL REP, Jg. 19, Nr. 2, S. 225-234. https://doi.org/10.1016/j.celrep.2017.03.046

APA

Spadaro, O., Camell, C. D., Bosurgi, L., Nguyen, K. Y., Youm, Y-H., Rothlin, C. V., & Dixit, V. D. (2017). IGF1 Shapes Macrophage Activation in Response to Immunometabolic Challenge. CELL REP, 19(2), 225-234. https://doi.org/10.1016/j.celrep.2017.03.046

Vancouver

Spadaro O, Camell CD, Bosurgi L, Nguyen KY, Youm Y-H, Rothlin CV et al. IGF1 Shapes Macrophage Activation in Response to Immunometabolic Challenge. CELL REP. 2017 Apr 11;19(2):225-234. https://doi.org/10.1016/j.celrep.2017.03.046

Bibtex

@article{90e61aa48a4f4c918819bd747f43fd0b,
title = "IGF1 Shapes Macrophage Activation in Response to Immunometabolic Challenge",
abstract = "In concert with their phagocytic activity, macrophages are thought to regulate the host immunometabolic responses primarily via their ability to produce specific cytokines and metabolites. Here, we show that IL-4-differentiated, M2-like macrophages secrete IGF1, a hormone previously thought to be exclusively produced from liver. Ablation of IGF1 receptors from myeloid cells reduced phagocytosis, increased macrophages in adipose tissue, elevated adiposity, lowered energy expenditure, and led to insulin resistance in mice fed a high-fat diet. The investigation of adipose macrophage phenotype in obese myeloid IGF1R knockout (MIKO) mice revealed a reduction in transcripts associated with M2-like macrophage activation. Furthermore, the MIKO mice infected with helminth Nippostrongylus brasiliensis displayed delayed resolution from infection with normal insulin sensitivity. Surprisingly, cold challenge did not trigger an overt M2-like state and failed to induce tyrosine hydroxylase expression in adipose tissue macrophages of control or MIKO mice. These results show that IGF1 signaling shapes the macrophage-activation phenotype.",
keywords = "Adipose Tissue, Adiposity, Animals, Cell Differentiation, Diet, High-Fat, Insulin Resistance, Insulin-Like Growth Factor I, Interleukin-4, Macrophages, Mice, Mice, Knockout, Nippostrongylus, Phagocytosis, Signal Transduction, Strongylida Infections, Journal Article",
author = "Olga Spadaro and Camell, {Christina D} and Lidia Bosurgi and Nguyen, {Kim Y} and Yun-Hee Youm and Rothlin, {Carla V} and Dixit, {Vishwa Deep}",
note = "Copyright {\textcopyright} 2017 The Author(s). Published by Elsevier Inc. All rights reserved.",
year = "2017",
month = apr,
day = "11",
doi = "10.1016/j.celrep.2017.03.046",
language = "English",
volume = "19",
pages = "225--234",
journal = "CELL REP",
issn = "2211-1247",
publisher = "Elsevier",
number = "2",

}

RIS

TY - JOUR

T1 - IGF1 Shapes Macrophage Activation in Response to Immunometabolic Challenge

AU - Spadaro, Olga

AU - Camell, Christina D

AU - Bosurgi, Lidia

AU - Nguyen, Kim Y

AU - Youm, Yun-Hee

AU - Rothlin, Carla V

AU - Dixit, Vishwa Deep

N1 - Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.

PY - 2017/4/11

Y1 - 2017/4/11

N2 - In concert with their phagocytic activity, macrophages are thought to regulate the host immunometabolic responses primarily via their ability to produce specific cytokines and metabolites. Here, we show that IL-4-differentiated, M2-like macrophages secrete IGF1, a hormone previously thought to be exclusively produced from liver. Ablation of IGF1 receptors from myeloid cells reduced phagocytosis, increased macrophages in adipose tissue, elevated adiposity, lowered energy expenditure, and led to insulin resistance in mice fed a high-fat diet. The investigation of adipose macrophage phenotype in obese myeloid IGF1R knockout (MIKO) mice revealed a reduction in transcripts associated with M2-like macrophage activation. Furthermore, the MIKO mice infected with helminth Nippostrongylus brasiliensis displayed delayed resolution from infection with normal insulin sensitivity. Surprisingly, cold challenge did not trigger an overt M2-like state and failed to induce tyrosine hydroxylase expression in adipose tissue macrophages of control or MIKO mice. These results show that IGF1 signaling shapes the macrophage-activation phenotype.

AB - In concert with their phagocytic activity, macrophages are thought to regulate the host immunometabolic responses primarily via their ability to produce specific cytokines and metabolites. Here, we show that IL-4-differentiated, M2-like macrophages secrete IGF1, a hormone previously thought to be exclusively produced from liver. Ablation of IGF1 receptors from myeloid cells reduced phagocytosis, increased macrophages in adipose tissue, elevated adiposity, lowered energy expenditure, and led to insulin resistance in mice fed a high-fat diet. The investigation of adipose macrophage phenotype in obese myeloid IGF1R knockout (MIKO) mice revealed a reduction in transcripts associated with M2-like macrophage activation. Furthermore, the MIKO mice infected with helminth Nippostrongylus brasiliensis displayed delayed resolution from infection with normal insulin sensitivity. Surprisingly, cold challenge did not trigger an overt M2-like state and failed to induce tyrosine hydroxylase expression in adipose tissue macrophages of control or MIKO mice. These results show that IGF1 signaling shapes the macrophage-activation phenotype.

KW - Adipose Tissue

KW - Adiposity

KW - Animals

KW - Cell Differentiation

KW - Diet, High-Fat

KW - Insulin Resistance

KW - Insulin-Like Growth Factor I

KW - Interleukin-4

KW - Macrophages

KW - Mice

KW - Mice, Knockout

KW - Nippostrongylus

KW - Phagocytosis

KW - Signal Transduction

KW - Strongylida Infections

KW - Journal Article

U2 - 10.1016/j.celrep.2017.03.046

DO - 10.1016/j.celrep.2017.03.046

M3 - SCORING: Journal article

C2 - 28402847

VL - 19

SP - 225

EP - 234

JO - CELL REP

JF - CELL REP

SN - 2211-1247

IS - 2

ER -