Macrophage and adipocyte interaction as a source of inflammation in kidney disease. Martos-Rus, C., Katz-Greenberg, G., Lin, Z., Serrano, E., Whitaker-Menezes, D., Domingo-Vidal, M., Roche, M., Ramaswamy, K., Hooper, D. C., Falkner, B., & Martinez Cantarin, M. P. Scientific Reports, 11(1):2974, February, 2021. Number: 1 Publisher: Nature Publishing Group![Macrophage and adipocyte interaction as a source of inflammation in kidney disease [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex In obesity, adipose tissue derived inflammation is associated with unfavorable metabolic consequences. Uremic inflammation is prevalent and contributes to detrimental outcomes. However, the contribution of adipose tissue inflammation in uremia has not been characterized. We studied the contribution of adipose tissue to uremic inflammation in-vitro, in-vivo and in human samples. Exposure to uremic serum resulted in activation of inflammatory pathways including NFκB and HIF1, upregulation of inflammatory cytokines/chemokines and catabolism with lipolysis, and lactate production. Also, co-culture of adipocytes with macrophages primed by uremic serum resulted in higher inflammatory cytokine expression than adipocytes exposed only to uremic serum. Adipose tissue of end stage renal disease subjects revealed increased macrophage infiltration compared to controls after BMI stratification. Similarly, mice with kidney disease recapitulated the inflammatory state observed in uremic patients and additionally demonstrated increased peripheral monocytes and inflammatory polarization of adipose tissue macrophages (ATMS). In contrast, adipose tissue in uremic IL-6 knock out mice showed reduced ATMS density compared to uremic wild-type controls. Differences in ATMS density highlight the necessary role of IL-6 in macrophage infiltration in uremia. Uremia promotes changes in adipocytes and macrophages enhancing production of inflammatory cytokines. We demonstrate an interaction between uremic activated macrophages and adipose tissue that augments inflammation in uremia.
@article{martos-rus_macrophage_2021,
title = {Macrophage and adipocyte interaction as a source of inflammation in kidney disease},
volume = {11},
copyright = {2021 The Author(s)},
issn = {2045-2322},
url = {https://www.nature.com/articles/s41598-021-82685-4},
doi = {10.1038/s41598-021-82685-4},
abstract = {In obesity, adipose tissue derived inflammation is associated with unfavorable metabolic consequences. Uremic inflammation is prevalent and contributes to detrimental outcomes. However, the contribution of adipose tissue inflammation in uremia has not been characterized. We studied the contribution of adipose tissue to uremic inflammation in-vitro, in-vivo and in human samples. Exposure to uremic serum resulted in activation of inflammatory pathways including NFκB and HIF1, upregulation of inflammatory cytokines/chemokines and catabolism with lipolysis, and lactate production. Also, co-culture of adipocytes with macrophages primed by uremic serum resulted in higher inflammatory cytokine expression than adipocytes exposed only to uremic serum. Adipose tissue of end stage renal disease subjects revealed increased macrophage infiltration compared to controls after BMI stratification. Similarly, mice with kidney disease recapitulated the inflammatory state observed in uremic patients and additionally demonstrated increased peripheral monocytes and inflammatory polarization of adipose tissue macrophages (ATMS). In contrast, adipose tissue in uremic IL-6 knock out mice showed reduced ATMS density compared to uremic wild-type controls. Differences in ATMS density highlight the necessary role of IL-6 in macrophage infiltration in uremia. Uremia promotes changes in adipocytes and macrophages enhancing production of inflammatory cytokines. We demonstrate an interaction between uremic activated macrophages and adipose tissue that augments inflammation in uremia.},
language = {en},
number = {1},
urldate = {2023-04-07},
journal = {Scientific Reports},
author = {Martos-Rus, Cristina and Katz-Greenberg, Goni and Lin, Zhao and Serrano, Eurico and Whitaker-Menezes, Diana and Domingo-Vidal, Marina and Roche, Megan and Ramaswamy, Kavitha and Hooper, Douglas C. and Falkner, Bonita and Martinez Cantarin, Maria P.},
month = feb,
year = {2021},
note = {Number: 1
Publisher: Nature Publishing Group},
keywords = {Cell biology, Immunology},
pages = {2974},
}
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We studied the contribution of adipose tissue to uremic inflammation in-vitro, in-vivo and in human samples. Exposure to uremic serum resulted in activation of inflammatory pathways including NFκB and HIF1, upregulation of inflammatory cytokines/chemokines and catabolism with lipolysis, and lactate production. Also, co-culture of adipocytes with macrophages primed by uremic serum resulted in higher inflammatory cytokine expression than adipocytes exposed only to uremic serum. Adipose tissue of end stage renal disease subjects revealed increased macrophage infiltration compared to controls after BMI stratification. Similarly, mice with kidney disease recapitulated the inflammatory state observed in uremic patients and additionally demonstrated increased peripheral monocytes and inflammatory polarization of adipose tissue macrophages (ATMS). In contrast, adipose tissue in uremic IL-6 knock out mice showed reduced ATMS density compared to uremic wild-type controls. 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