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Expression Data from murine control and IL6ralpha-deficient macrophages stimulated with Interleukin-6

ABSTRACT: IL-6 induces IL4ralpha expression in macrophages. This mechanism is necessary to promote macrophage polarization towards an M2-phenotype and is crucial to limit the inflammatory response both upon obesity and LPS-endotoxemia. In this dataset, we include the expression data obtained from primary murine bone marrow-derived macrophages from control and IL6ralpha-deficient macrophages (n=4vs4) stimulated with interleukin-6 (IL-6) 8 samples were analyzed to compare control and IL6ralpha-deficient macrophages for their gene expression profiles upon stimulation with IL-6

ORGANISM(S): Mus musculus

SUBMITTER: Jan Mauer

PROVIDER: E-GEOD-47426 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Signaling by IL-6 promotes alternative activation of macrophages to limit endotoxemia and obesity-associated resistance to insulin.

Mauer Jan J Chaurasia Bhagirath B Goldau Julia J Vogt Merly C MC Ruud Johan J Nguyen Khoa D KD Theurich Sebastian S Hausen A Christine AC Schmitz Joel J Brönneke Hella S HS Estevez Emma E Allen Tamara L TL Mesaros Andrea A Partridge Linda L Febbraio Mark A MA Chawla Ajay A Wunderlich F Thomas FT Brüning Jens C JC

Nature immunology 20140330 5

Obesity and resistance to insulin are closely associated with the development of low-grade inflammation. Interleukin 6 (IL-6) is linked to obesity-associated inflammation; however, its role in this context remains controversial. Here we found that mice with an inactivated gene encoding the IL-6Rα chain of the receptor for IL-6 in myeloid cells (Il6ra(Δmyel) mice) developed exaggerated deterioration of glucose homeostasis during diet-induced obesity, due to enhanced resistance to insulin. Tissues ...[more]

PMID: 24681566

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