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

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

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...

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Bibliographic Details
Published in:Cell proliferation Vol. 50; no. 5
Main Authors: Magnuson, A. M., Regan, D. P., Fouts, J. K., Booth, A. D., Dow, S. W., Foster, M. T.
Format: Journal Article
Language:English
Published: England John Wiley & Sons, Inc 01-10-2017
John Wiley and Sons Inc
Subjects:
Adipose tissue
Adipose Tissue - cytology
Adipose Tissue - immunology
Adipose Tissue - pathology
Animals
Antigen-presenting cells
CD8 antigen
Cell number
Cell Survival
Cytology
Cytometry
Diet, High-Fat - adverse effects
Flow cytometry
Health risks
Histopathology
Hyperplasia
Hyperplasia - etiology
Hyperplasia - immunology
Hyperplasia - pathology
Immune response
Immune system
Immunity, Cellular
Immunofluorescence
Immunoregulation
Inflammation
Lymph nodes
Lymph Nodes - immunology
Lymph Nodes - pathology
Lymphatic system
Lymphocytes
Lymphocytes T
Macrophages
Male
Mice, Inbred C57BL
Obesity
Obesity - complications
Obesity - etiology
Obesity - immunology
Obesity - pathology
Original
Populations
Rodents
Spleen - immunology
Spleen - pathology
T cell receptors
Thymus Gland - immunology
Thymus Gland - pathology
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Summary: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 towards 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.
Bibliography:Funding information
This work was supported by the National Institutes of Health [grant numbers P30 DK048520 and R03 DK099425]
ISSN:0960-7722
1365-2184
DOI:10.1111/cpr.12365