Chronic cold stress in mice induces a regulatory phenotype in macrophages: Correlation with increased 11β-hydroxysteroid dehydrogenase expression

Sesti-Costa, Renata; Ignacchiti, M.D.C.; Chedraoui-Silva, S.; Marchi, Larissa Fávaro; Mantovani, Bernardo

doi:10.1016/j.bbi.2011.07.234

Cited by 45 publications

(22 citation statements)

References 60 publications

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“…Regulation of IL-10 or TNF produced by macrophages could improve immunotherapy of tumors by reducing unwanted IL-10 production and induction of immunosuppressive macrophages. 47,48 Likewise, controlled induction of IL-10 or TNF in diabetes could improve wound healing or the regulation of the autoimmune response. 49,50 …”

Section: Discussionmentioning

confidence: 99%

The DNA-binding factor Ctcf critically controls gene expression in macrophages

et al. 2013

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Section: Discussionmentioning

confidence: 99%

The DNA-binding factor Ctcf critically controls gene expression in macrophages

et al. 2013

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“…18) Moreover, it has been reported that chronic cold stress induced a regulatory phenotype in macrophages, characterized by diminished phagocytic ability, decreased TNF-α and IL-6, and increased IL-10 production. 19) * To whom correspondence should be addressed. e-mail: ynakatani@iuhw.ac.jp…”

mentioning

confidence: 99%

Corticosterone Suppresses the Proliferation of RAW264.7 Macrophage Cells via Glucocorticoid, But Not Mineralocorticoid, Receptor

Nakatani

Amano

Takeda

2013

Biological & Pharmaceutical Bulletin

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Macrophages are white blood cells within tissues that are produced by monocytes and help to protect against infection by bacteria through phagocytosis. Several studies have shown a correlation between the state of depression and abnormalities in the immune response. Corticosterone (CORT), which is often referred to as the stress hormone, is a well-known regulator of peripheral immune responses and also shows anti-inflammatory properties in the body. However, it is still unclear how CORT regulates macrophage function. In this study, we focused on the effects of CORT on the proliferation and survival of macrophage cells using the macrophage cell line RAW264.7. Under treatment with 10 µm CORT for 24 h, the proliferation of RAW264.7 cells decreased to 73.6% of that in the control. Moreover, this inhibition was blocked by treatment with mifepristone, a glucocorticoid receptor (GR) antagonist, but not by spironolactone, a mineralocorticoid receptor (MR) antagonist. In an lactate dehydrogenase (LDH) assay, CORT did not show any cytotoxic effect on RAW264.7 cells. JC-1 cell staining also showed that CORT did not influence mitochondrial dysfunction in RAW264.7 cells. In an investigation of the modulation of a signaling cascade by CORT, treatment with CORT promoted the translocation of GR, but not MR, from the cytosol to the nucleus in RAW264.7 cells. In conclusion, our findings suggest that CORT suppresses the proliferation of RAW264.7 cells by controlling the transcription of a particular gene, which is related to cell proliferation, through the formation of a CORT-GR complex.Key words glucocorticoid; mineralocorticoid; corticosterone; RAW264.7; mifepristone; spironolactone Corticosterone (CORT), which is classified as a steroid hormone, is an adrenal corticosteroid that plays a role in a wide range of phenomena, such as the regulation of glucose metabolism, the reaction of the immune system and the stress response. CORT is one of the main corticosteroids in rodents. There are two types of adrenal corticosteroid receptors: type II, or glucocorticoid receptor (GR), and type I, or mineralocorticoid receptor (MR).1,2) It has been demonstrated that CORT has greater affinity for MR than for GR. 3,4) In general, both GR and MR are localized in the cytosol. It has been demonstrated that a ligand-steroid hormone receptor complex forms a homodimer together with another chaperon protein once CORT binds to steroid hormone receptor. After it forms a homodimer complex, this complex translocates from the cytosol to the nucleus and binds to a particular motif of DNA to regulate DNA transcription.5) In the case of GR, intracellular GR is inactivated by the formation of complexes with several proteins, such as heat-shock proteins.6,7) After the active ligand-steroid hormone receptor complex forms a homodimer and translocates to the nucleus from the cytosol, it modulates the transcriptional responses of inflammatory genes, either by binding directly to DNA or by cooperating with some other protein or signal cascade, such as nuclear facto...

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“…Resting macrophages stimulated spleen cells to produce regulatory cytokines, and an immunosuppressive state that impaired cold stressed mice to control Trypanosoma cruzi proliferation [718]. These regulatory effects correlated with an increase in macrophage expression of 11β-hydroxysteroid dehydrogenase, an enzyme that converts inactive glucocorticosteroid into its active form [718].…”

Section: Prevention Of Hypoglycemia-induced Neuronal Death By Hypothementioning

confidence: 95%

“…In mice, chronic cold stress induced a regulatory phenotype in macrophages, characterized by diminished phagocytic ability, decreased TNF-α and IL-6 and increased IL-10 production [718]. Resting macrophages stimulated spleen cells to produce regulatory cytokines, and an immunosuppressive state that impaired cold stressed mice to control Trypanosoma cruzi proliferation [718].…”

Section: Prevention Of Hypoglycemia-induced Neuronal Death By Hypothementioning

confidence: 99%

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Pr¹,

ota²

2013

J Diabetes Metab

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Recently, it was suggested that maternal T and potentially B cells transferred during pregnancy and/or the breast milk feeding and their encounter with the antigen in mesenteric lymph nodes might play a role in development of type 1 diabetes mellitus (T1DM). T. gondii infection during gestation and/or after birth may be responsible for development of both T1DM and T2DM in children, adolescents and adults because: a) maternal microchimerism in peripheral blood was demonstrated to be significantly higher in patients with T1DM compared to unaffected siblings and healthy subjects, b) transmission of T. gondii as a Trojan horse in various types of eukaryotic cells, including T and B lymphocytes, c) swallowing by the fetus of amniotic fluid containing infected leukocytes and other cells, d) elimination of T. gondii in the breast milk during lactation, e) involvement of mesenteric lymph nodes after oral infection with the parasite, and f) damage of the myenteric neurons during infection with the parasite in both the animals with streptozotocin-induced diabetes and diabetic patients. Moreover, a significantly lower occurrence of antibodies against T. gondii found in the sera of patients with T1DM compared with their first-degree family members or healthy controls may be due to their T and/or B cell exhaustion perspective caused by chronic infection with the parasite. This suggestion may be supported by the finding that latent toxoplasmosis was associated with markedly reduced lymphocyte B-cell counts responsible for production of antibodies, markedly lower serum IgG, IgM, and IgA levels, and a significant suppression of IL-2. On the other hand, patients with T2DM had increased anti-T. gondii antibodies significantly more frequently than respective controls. Impaired vascular endothelial function characteristic for the patients with diabetes mellitus may be at least in part due to the preferential T. gondii infection of endothelial cells. Vitamin D and minocycline exerted beneficial effects on development and clinical course of diabetes mellitus probably because of their immunomodulatory and antitoxoplasmatic activities. These data strongly suggest that the parasite play an important role in development of both types of diabetes mellitus.

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Chronic cold stress in mice induces a regulatory phenotype in macrophages: Correlation with increased 11β-hydroxysteroid dehydrogenase expression

Cited by 45 publications

References 60 publications

The DNA-binding factor Ctcf critically controls gene expression in macrophages

The DNA-binding factor Ctcf critically controls gene expression in macrophages

Corticosterone Suppresses the Proliferation of RAW264.7 Macrophage Cells via Glucocorticoid, But Not Mineralocorticoid, Receptor

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

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