Obesity Accelerates Age Defects in Mouse and Human B Cells.

Daniela Frasca,Bonnie B Blomberg

doi:10.3389/fimmu.2020.02060

Abstract

Obesity, similar to aging, is associated with chronic low-grade systemic inflammation, known as inflammaging, and represents a significantly higher risk for developing chronic diseases typical of old age. Immune cells are recruited to the obese adipose tissue (AT) by chemotactic molecules secreted by non-immune and immune cells in the AT, both contributing to the release of several pro-inflammatory mediators that fuel local and systemic inflammation, to the refractory response of immune cells to further in vivo and in vitro stimulation and to the induction of autoimmune B cells with potentially pathogenic repertoires. In terms of molecular mechanisms involved, leptin, an adipokine secreted primarily by adipocytes, has been proposed to be involved in the reduced generation of protective antibodies, and in the increased generation of autoimmune antibodies, further supporting the concept that obesity accelerates age defects. Leptin has also been shown to induce intrinsic B cell inflammation and B cell immunosenescence. The results presented in this review highlight the importance of weight reduction programs to improve immunity and reduce the risk for developing chronic diseases in obese and older individuals.

Highlights

Obesity, defined as body-mass index (BMI) ≥ 30 kg/m2 by CDC and WHO, is an increasing health concern that affects young [1] and older adults [2], and has reached pandemic proportions
One of the reasons is because obesity, similar to aging, is an inflammatory condition associated with chronic low-grade systemic inflammation, inflammaging [11], which is negatively associated with a functional immune system, healthspan and longevity in both mice and humans [12]
Initial studies have indicated that mice fed high-fat diet (HFD) secrete more pro-inflammatory cytokines (IL-6/TNF-α) than B cells from mice fed normal-fat diet (NFD), contributing to the higher levels of systemic inflammation observed in mice fed HFD [47] and in aged mice [48]

Summary

Obesity Accelerates Age Defects in Mouse and Human B Cells

Reviewed by: Gerardo Ferbeyre, Université de Montréal, Canada Saame Raza Shaikh, The University of North Carolina at Chapel Hill, United States. Similar to aging, is associated with chronic low-grade systemic inflammation, known as inflammaging, and represents a significantly higher risk for developing chronic diseases typical of old age. Immune cells are recruited to the obese adipose tissue (AT) by chemotactic molecules secreted by non-immune and immune cells in the AT, both contributing to the release of several pro-inflammatory mediators that fuel local and systemic inflammation, to the refractory response of immune cells to further in vivo and in vitro stimulation and to the induction of autoimmune B cells with potentially pathogenic repertoires. In terms of molecular mechanisms involved, leptin, an adipokine secreted primarily by adipocytes, has been proposed to be involved in the reduced generation of protective antibodies, and in the increased generation of autoimmune antibodies, further supporting the concept that obesity accelerates age defects. The results presented in this review highlight the importance of weight reduction programs to improve immunity and reduce the risk for developing chronic diseases in obese and older individuals

INTRODUCTION

EFFECTS OF OBESITY ON MOUSE B CELLS

EFFECTS OF OBESITY ON HUMAN B CELLS

Findings

AUTHOR CONTRIBUTIONS