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Transmission Electron Microscopy Analysis of Visceral and Subcutaneous Lymph Nodes: High Fat Diet‐Induced Morphological Changes
Author(s) -
Foster Michelle,
Vanderpool Kimberly
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb515
Subject(s) - lymph , immune system , adipose tissue , lymphatic system , inflammation , acquired immune system , pathology , immunity , biology , medicine , immunology , endocrinology
Inflammation, induced by excessive adipose tissue accumulation, appears to link obesity to disease risk yet little attention has been devoted to the lymphoid tissues embedded within adipose tissue. These structures are the primary site for the development of protective immunity, including antibody and cellular immune responses. Hence, any disease process that affects lymphoid tissues will also directly impact immunity, including responses to pathogens, infections, cancer and vaccines. We examined how obesity alters secondary lymphatic tissue structure and immune cells encapsulated within. 4 month C57BL/6 male mice were fed standard rodent Chow (n = 3) (Harlan – 7002: 18% of calories from fat and 49% from carbohydrates) or Western high fat diet (n = 3) (HFD, Harlan ‐ TD.88137: 42% of calories primarily from saturated fat from milkfat and 42% from sucrose) for 6 months. Body mass was recorded for the duration of the study. Because visceral, but not subcutaneous, adipose tissue accumulation is highly associated with metabolic disease, visceral and subcutaneous lymph nodes were analyzed via transmission electron microscopy. HFD‐induced obesity caused numerous morphology changes to immune cells and sinus space in both visceral and subcutaneous lymph nodes. Lymph nodes of HFD mice contained large amounts of cellular debris indicative of damaged or dead cells. Large engulfing macrophages where associated with debris dense regions. HFD intake also increased collagen and microfibrils within lymph nodes. These structural proteins are products of dysregulated enlarged fibroblastic reticular cells (FRCs). Under normal conditions, FRC network maintains T cell homeostasis and cellular interactions needed for a proper immune response. Disruption of this network was associated with increased sinus spacing between immune cells. Overall, HFD‐induced obesity caused cellular death and macrophage activation. We postulate obesity associated inflammation causes FRCs to‐induce fibrosis within lymph nodes and likely contributes to increased sinus spacing and subsequently reduced immune cell interactions. The consequential outcomes on immune regulation would likely contribute to the immunosuppression and lymphatic vessel dysfunction demonstrated to occur during obesity. Support or Funding Information NIH R03DK099425