Effects of Cold Stress, Corticosterone and Catecholamines on Phagocytosis in Mice: Differences between Resting and Activated Macrophages

Baccan, Gyselle Chrystina; Sesti-Costa, Renata; Chedraoui-Silva, S.; Mantovani, Bernardo

doi:10.1159/000292058

Cited by 15 publications

(10 citation statements)

References 68 publications

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“…One study of murine wound showed that both low (1 x 10 -9 M) and high (1 x 10 -6 M) doses of NE suppressed wound macrophage phagocytic efficiency [12]. However, studies of mouse peritoneal macrophages found that lower doses of NE enhanced phagocytosis and cytokine production, whereas higher doses of NE have less effectiveness [13,14]. Macrophages are major producers of pro-inflammatory mediators during burn injury and sepsis [10].…”

Section: Introductionmentioning

confidence: 99%

Norepinephrine Inhibits Macrophage Migration by Decreasing CCR2 Expression

2013

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Increased incidences of infectious and septic complications during post-burn courses represent the main contributor to burn injury mortality. Sustained increases in catecholamine levels, especially norepinephrine (NE), contribute to immune disturbances in severely burned patients. The precise mechanisms underlying NE-mediated immunoregulation are not fully understood. Here we hypothesize that persistently elevated NE levels are associated with immunodysfunctions. We examined the effects of NE on the phenotype and functions of bone marrow-derived macrophages (BMMs). Whole mouse bone marrow cells were treated in vitro with 40 ng/mL of M-CSF and with 1 x 10-6 M or 1 x 10-8 M of NE or without NE for 7 days; cells were collected and stained with antibodies for CD11b, F4/80, MHC II and the inflammatory CC chemokine receptor 2 (CCR2). We found 1 x 10-6 M of NE inhibited MHC II and CCR2 expression on CD11b+/F4/80+ BMM cells. It also inhibited BMM proliferation by inhibiting CSF-1R expression. On the contrary, 1 x 10-8 M of NE slightly increased both MHC II and CCR2 expression on CD11b+/F4/80+ BMM cells but inhibited CD11b+/F4/80+ BMM proliferation. MCP-1 based migration assay showed that the migration of 1 x 10-6 M of NE-treated BMM toward MCP-1 was significantly decreased compared to BMM without NE treatment. Both 1 x 10-8 M and 1 x 10-6 M of NE enhanced TNF-α production and phagocytosis of FITC-Dextran. Intracellular staining of transcriptional factor MafB showed that 1 x 10-6 M of NE treatment enhanced its expression, whereas 1 x 10-8 M of NE decreased expression. Stimulation with LPS in the last 24-hours of BMM culture further decreased CCR2 and MHC II expression of these BMM, suggesting the synergistic effect of LPS and NE on macrophage. Our results demonstrate that NE regulates macrophage differentiation, proliferation and function, and may play a critical role in the dysfunctional immune response post-burn.

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Section: Introductionmentioning

confidence: 99%

Norepinephrine Inhibits Macrophage Migration by Decreasing CCR2 Expression

2013

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“…24) Moreover, in resting macrophages, corticosterone decreased phagocytosis mediated by Fc-gamma and mannose and beta-glucan receptors, while catecholamines had no effect. 25,26) There is also direct evidence that rat macrophage cells, which were pretreated with CORT, reduced the production of TNF-α by the treatment with lipopolysaccharides. 27) These findings suggest that glucocorticoids released in response to stress stimuli suppress the immune response by directly changing the activity and phenotype of macrophage cells.…”

Section: Discussionmentioning

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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“…Besides, possible changes in the gut proinflammatory cytokine microenvironment of fish fed MOS (Torrecillas, Makol, Betancor, Ganga, Caballero, Montero & Izquierdo, personal observation), which could influence the leucocyte′s functional capacity to respond to a treatment with glucocorticoids (Heasman et al. 2004), or a possible change in the response of the activated phagocytes by mannose receptors (MRs) (Baccan et al. 2010) to glucocorticoids and its contribution to the lower disease incidence found in the present study for infected groups fed MOS should not be discarded.…”

Section: Discussionmentioning

confidence: 99%

Effects on mortality and stress response in European sea bass, Dicentrarchus labrax (L.), fed mannan oligosaccharides (MOS) after Vibrio anguillarum exposure

Torrecillas¹,

Makol²,

Caballero³

et al. 2012

Journal of Fish Diseases

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The effects of dietary mannan oligosaccharides (MOS; 4 g kg−1; Bio‐Mos, Alltech Inc, USA) in diets for European sea bass, Dicentrarchus labrax (L.), juveniles in relation to disease and stress resistance, combining intestinal infection with Vibrio anguillarum and stress challenge by confinement, were assessed in this study. After 8 weeks of MOS supplementation, fish were exposed to a pathogen challenge test against V. anguillarum by direct gut inoculation combined with a confinement stressor panel. Cumulative mortality of fish fed MOS caused by anally inoculated V. anguillarum decreased from 66% to 12.5% and from 54.1% to 25% in infected and infected + stressed fish, respectively, compared to fish fed control diet. Results for European sea bass revealed a positive effect of MOS dietary inclusion on disease resistance, in terms of cumulative mortality, against gut inoculated V. anguillarum, as well as reduced effects of stress on microbiota diversity. Both of these findings, together with the enhanced innate immune response and the higher gut mucus production and density of eosinophil granulocytes in gut mucosa obtained in previous studies after MOS supplementation (Torrecillas et al. 2007, 2011a,b) suggest that general reinforcement of the innate immune system, and particularly of the intestinal barrier efficiency, is the main defence mechanism of European sea bass fed MOS against pathogenic microorganisms.

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Effects of Cold Stress, Corticosterone and Catecholamines on Phagocytosis in Mice: Differences between Resting and Activated Macrophages

Cited by 15 publications

References 68 publications

Norepinephrine Inhibits Macrophage Migration by Decreasing CCR2 Expression

Norepinephrine Inhibits Macrophage Migration by Decreasing CCR2 Expression

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

Effects on mortality and stress response in European sea bass, Dicentrarchus labrax (L.), fed mannan oligosaccharides (MOS) after Vibrio anguillarum exposure

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