Adipose tissue and the immune system

Pond, Caroline M.

doi:10.1016/j.plefa.2005.04.005

Cited by 184 publications

(127 citation statements)

References 94 publications

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“…Thus, the fat itself could play a critical role in our observations, because the white adipose tissue of ob/ob mice display increased proportion of n-6 fatty acids (49) that have been reported to increase DC recruitment (50). In addition to being involved in the alteration of DC steady-state number we presently describe in ob/ob mice, white adipose tissue could also participate to their impaired functionality because membrane fatty acid composition of DCs highly depends on surrounding adipocytes and any alteration in this composition affects their functionality (51,52), like the decreased KLH response we observed. Finally, to go further with "the altered environment hypothesis," we confirmed through the TNF-␣-induced LC migration test, that those cells had no intrinsic migratory defect.…”

Section: Discussionmentioning

confidence: 85%

Impairment of Dendritic Cell Functionality and Steady-State Number in Obese Mice

Macia

Delacre

Abboud

et al. 2006

The Journal of Immunology

124

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There is a finely tuned interplay between immune and neuroendocrine systems. Metabolic disturbances like obesity will have serious consequences on immunity both at the cellular and at the cytokine expression levels. Our in vivo results confirm the immune deficiency of ob/ob mice, leptin deficient and massively obese, characterized by a reduced Ag-specific T cell proliferation after keyhole limpet hemocyanin immunization. In this report, we show that dendritic cells (DCs), major APCs involved in T lymphocyte priming, are affected in obese mice. Both their function and their steady-state number are disturbed. We demonstrate that DCs from ob/ob mice are less potent in stimulation of allogenic T cells in vitro. This impaired functionality is not associated with altered expression of phenotypic markers but with the secretion of immunosuppressive cytokines such as TGF-β. Moreover, we show increased in vivo steady-state number of epidermal DCs in ob/ob mice, which is not due to a migratory defect. The ob/ob mice are characterized by the absence of functional leptin, a key adipokine linking nutrition, metabolism, and immune functions. Interestingly, intradermal injection of leptin is able to restore epidermal DC number in obese mice. Thus, DCs might be directly sensitive to metabolic disturbances, providing a partial explanation of the immunodeficiency associated with obesity.

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Section: Discussionmentioning

confidence: 85%

Impairment of Dendritic Cell Functionality and Steady-State Number in Obese Mice

Macia

Delacre

Abboud

et al. 2006

The Journal of Immunology

124

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“…Therefore, the cells of the lymph node are supplied with specialised free fatty acids by the perinodal adipocytes, and dendritic cells from the lymph nodes are able to modulate lipolysis of the surrounding adipose tissue. 86 Furthermore, the adipokine, leptin has been shown to have effects on immune system functionality. Subjects with a leptin gene mutation have very low serum leptin levels and reduced numbers of CD 4 + T cells and low T-cell proliferation rates.…”

Section: Adiposity and Insulin Resistance As A Biological Advantagementioning

confidence: 99%

Once fat was fat and that was that : our changing perspectives on adipose tissue

Ferris

Crowther

2011

CardioVascular Journal of Africa

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Past civilisations saw excess body fat as a symbol of wealth and prosperity as the general population struggled with food shortages and famine. Nowadays it is recognised that obesity is associated with co-morbidities such as cardiovascular disease and diabetes. Our views on the roll of adipose tissue have also changed, from being solely a passive energy store, to an important endocrine organ that modulates metabolism, immunity and satiety. The relationship between increased visceral adiposity and obesity-related co-morbidities has lead to the recognition that variation in fat distribution contributes to ethnic differences in the prevalence of obesity-related diseases. Our current negative view of adipose tissue may change with the use of pluripotent adipose-derived stromal cells, which may lead to future autologous stem cell therapies for bone, muscle, cardiac and cartilage disorders. Here, we briefly review the concepts that adipose tissue is an endocrine organ, that differences in body fat distribution underline the aetiology of obesity-related co-morbidities, and the use of adipose-derived stem cells for future therapies.

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“…AT has been described as a heterogeneous tissue that possesses marked anatomically‐related depot specialization in regard to many parameters, including cellularity, form of growth and expansion, metabolism, production of and response to cytokines, hormones, density and distribution of innervation, as well as to fatty acid composition (reviewed by Pond19). Several chronic diseases, such as obesity,20 metabolic syndrome and lipodystrophy,21 induce AT remodelling, involving two major processes: adipose cell morphometric changes (hypertrophy or atrophy) and immune cells accumulation.…”

Section: Introductionmentioning

confidence: 99%

Cachexia-associated adipose tissue morphological rearrangement in gastrointestinal cancer patients

Batista

Henriques

Neves

et al. 2015

Journal of Cachexia, Sarcopenia and Muscle

106

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Background and aimsCachexia is a syndrome characterized by marked involuntary loss of body weight. Recently, adipose tissue (AT) wasting has been shown to occur before the appearance of other classical cachexia markers. We investigated the composition and rearrangement of the extracellular matrix, adipocyte morphology and inflammation in the subcutaneous AT (scAT) pad of gastrointestinal cancer patients.MethodsSurgical biopsies for scAT were obtained from gastrointestinal cancer patients, who were signed up into the following groups: cancer cachexia (CC, n = 11), weight‐stable cancer (WSC, n = 9) and weight‐stable control (non‐cancer) (control, n = 7). The stable weight groups were considered as those with no important weight change during the last year and body mass index <25 kg/m2. Subcutaneous AT fibrosis was quantified and characterized by quantitative PCR, histological analysis and immunohistochemistry.ResultsThe degree of fibrosis and the distribution and collagen types (I and III) were different in WSC and CC patients. CC patients showed more pronounced fibrosis in comparison with WSC. Infiltrating macrophages surrounding adipocytes and CD3 Ly were found in the fibrotic areas of scAT. Subcutaneous AT fibrotic areas demonstrated increased monocyte chemotactic protein 1 (MCP‐1) and Cluster of Differentiation (CD)68 gene expression in cancer patients.ConclusionsOur data indicate architectural modification consisting of fibrosis and inflammatory cell infiltration in scAT as induced by cachexia in gastrointestinal cancer patients. The latter was characterized by the presence of macrophages and lymphocytes, more evident in the fibrotic areas. In addition, increased MCP‐1 and CD68 gene expression in scAT from cancer patients may indicate an important role of these markers in the early phases of cancer.

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Adipose tissue and the immune system

Cited by 184 publications

References 94 publications

Impairment of Dendritic Cell Functionality and Steady-State Number in Obese Mice

Impairment of Dendritic Cell Functionality and Steady-State Number in Obese Mice

Once fat was fat and that was that : our changing perspectives on adipose tissue

Cachexia-associated adipose tissue morphological rearrangement in gastrointestinal cancer patients

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