Diet‐induced obesity causes visceral, but not subcutaneous, lymph node hyperplasia via increases in specific immune cell populations

Abstract

Objectives The spatial proximity of adipose depots to secondary lymph nodes allows a unique relation between the two systems. Obesity, predominately-visceral adiposity, links to numerous diseases, hence we postulate that secondary lymphatics within this region contributes to disease risk. Material and Methods Male C57BL/6 mice were fed standard chow (18% kcal fat) or Western diet (45% kcal fat) for 7 weeks. Visceral and subcutaneous lymph nodes and associated adipose depots they occupy were excised. Lymph node morphology and resident immune cell populations were characterized via histopathology, immunofluorescence, and flow cytometry. Adipose tissue immune cell populations were also characterized. Results Obesity caused lymph node expansion, increased viable cell number, and deviations in immune cell populations. These alterations were exclusive to visceral lymph nodes. Notably, pro-inflammatory antigen presenting cells and regulatory T cells increased in number in the visceral lymph node. Obesity, however, reduced T regulatory cells in visceral lymph nodes. The visceral adipose depot also had greater reactivity toward HFD than subcutaneous, with a greater percent of macrophages, dendritic and CD8+ T cells. Immune cell number, in both the visceral and subcutaneous, however decreased as adipose depots enlarged. Conclusion Overall, HFD has a greater influence on visceral cavity than the subcutaneous. In the visceral lymph node, but not subcutaneous, HFD-induced obesity decreased cell populations that suppressed immune function while increasing those that regulate/activate immune response.

Anti-Obesity Effects of the Flower of Prunus persica in High-Fat Diet-Induced Obese Mice

“…HFD also induces spleen enlargement via sinusoidal dilatation and extracellular deposits, such as lipid and hemosiderin [34,35]. This enlarged spleen, as the main immune organ, produces higher levels of inflammatory cytokines and shows increased T cell proliferation, contributing to chronic systemic inflammation [36]. Our results suggest that PPF might counteract obesity-induced fatty liver and splenomegaly.…”

Immune cell populations residing in mesenteric adipose depots and mesenteric lymph nodes of lean dairy cows

“…Regulatory immune phenotype(s) in the MLN could generate the anti-inflammatory environments supporting the mucosal permeability barrier integrity that prevents trans-mucosal translocation of commensal bacterial elements triggering adipose inflammation (Cani et al, 2007(Cani et al, , 2008. Although the majority of immune signals from the intestinal mucosa influence cellular structure and function in the MLN, experimental evidence shows that the phenotypic structure of the MLN is also transformed by signals arising from the mesenteric adipose depot (Magnuson et al, 2017). Even within the limited realm of available reagents, results from this study set the foundation upon which the functional phenotypes of regulatory/anti-inflammatory elements in fat and the intestine can be explored.…”

“…Populations of proinflammatory macrophages, dendritic cells, and T lymphocytes increase in MLN of adipose depots with hypertrophied adipocytes. Coincidently, the size of the Treg population decreases in these MLN (Magnuson et al, 2017). The pivotal function of MLN is to sustain immune homeostasis in the intestinal mucosa and secondarily to orchestrate steady-state homeostasis in the mesenteric adipose.…”

Innate Immune System Orchestrates Metabolic Homeostasis and Dysfunction in Visceral Adipose Tissue During Obesity

“…Recently, innate immune cells in VAT have been implicated in the regulation of adipose tissue homeostasis and low-grade inflammation during obesity. Most of such cells are adiposetissue-resident cells that have distinct phenotypes and functions and are altered in numbers or activity during significant changes in the VAT environment (2). Among these cells, VAT-resident innate immune cell types, group 2 innate lymphoid cells (ILC2s), eosinophils, invariant natural killer T cells (iNKTs), and macrophages play key roles in maintaining type II immune state in VAT homeostasis.…”