GM-CSF- and M-CSF-dependent macrophage phenotypes display differential dependence on Type I interferon signaling

Fleetwood, Andrew J.; Dinh, Hang Thuy; Cook, Andrew D.; Hertzog, Paul J.; Hamilton, John A.

doi:10.1189/jlb.1108702

Cited by 254 publications

(262 citation statements)

References 64 publications

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“…This confirms that LPS tolerance is a transient macrophage-activation state in both mouse and human macrophage/monocyte cells (Fig. 1B, 1C), in agreement with previous in vitro and in vivo studies (8,(27)(28)(29)38).…”

Section: Recovery From Lps Tolerance Involves a Global Shift In The Tsupporting

confidence: 80%

Identification of a Unique Hybrid Macrophage-Polarization State following Recovery from Lipopolysaccharide Tolerance

O’Carroll

Fagan

Shanahan

et al. 2014

The Journal of Immunology

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LPS tolerance is an essential immune-homeostatic response to repeated exposure to LPS that prevents excessive inflammatory responses. LPS tolerance induces a state of altered responsiveness in macrophages, resulting in repression of proinflammatory gene expression and increased expression of factors that mediate the resolution of inflammation. In this study, we analyzed the transcriptional plasticity of macrophages following LPS tolerance using genome-wide transcriptional profiling. We demonstrate that LPS tolerance is a transient state and that the expression of proinflammatory genes is restored to levels comparable to the acute response to LPS. However, following recovery from LPS tolerance a number of genes remained locked in a tolerizable state, including IL-33, CD86, IL-10, and NFIL3. Furthermore, we identified of a number of genes uniquely induced following recovery from LPS tolerance. Thus, macrophages adopt a unique transcriptional profile following recovery from LPS tolerance and have a distinct expression pattern of regulators of Ag presentation, antiviral responses, and transcription factors. Our data suggest that recovery from LPS tolerance leads to a hybrid macrophage activation state that is proinflammatory and microbicidal in nature but that possesses a regulatory anti-inflammatory profile distinct from that of LPS-tolerant and LPS-activated macrophages.

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Section: Recovery From Lps Tolerance Involves a Global Shift In The Tsupporting

confidence: 80%

Identification of a Unique Hybrid Macrophage-Polarization State following Recovery from Lipopolysaccharide Tolerance

O’Carroll

Fagan

Shanahan

et al. 2014

The Journal of Immunology

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“…The non-adherent cells and loosely attached cells were washed by swirling the plates on day 3, 5, 7, and 9 30,31 . The purity of BMDMs was more than 95% (Supplementary Figure 1A).…”

Section: Cell Preparationmentioning

confidence: 99%

TSC1 controls IL-1β expression in macrophages via mTORC1-dependent C/EBPβ pathway

et al. 2015

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The tuberous sclerosis complex 1 (TSC1) is a tumor suppressor that inhibits the mammalian target of rapamycin (mTOR), which serves as a key regulator of inflammatory responses after bacterial stimulation in monocytes, macrophages, and primary dendritic cells. Previous studies have shown that TSC1 knockout (KO) macrophages produced increased inflammatory responses including tumor necrosis factor-a (TNF-a) and IL-12 to pro-inflammatory stimuli, but whether and how TSC1 regulates pro-IL-1b expression remains unclear. Here using a mouse model in which myeloid lineage-specific deletion of TSC1 leads to constitutive mTORC1 activation, we found that TSC1 deficiency resulted in impaired expression of pro-IL-1b in macrophages following lipopolysaccharide stimulation. Such decreased pro-IL-1b expression in TSC1 KO macrophages was rescued by reducing mTORC1 activity with rapamycin or deletion of mTOR. Rictor deficiency has no detectable effect on pro-IL-1b synthesis, suggesting that TSC1 positively controls pro-IL-1b expression through mTORC1 pathway. Moreover, mechanism studies suggest that mTORC1-mediated downregulation of the CCAAT enhancer-binding protein (C/EBPb) critically contributes to the defective pro-IL-1b expression. Overall, these findings highlight a critical role of TSC1 in regulating innate immunity by control of the mTOR1-C/EBPb pathway. Cellular & Molecular Immunology

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“…It was involved in regulating the numbers and function of macrophage lineage populations and have been shown to contribute to macrophage heterogeneity [2]. However, it can act on macrophage populations and are implicated in host defense and inflammation [3].…”

Section: Introductionmentioning

confidence: 99%

Impact of Serum Granulocyte-Macrophage Colony-Stimulating Factor Levels among Diabetes Patients in Hilla City - Iraq

Al-Hassnawi¹,

Al-Thaheb²,

Al-Dahmoshi³

et al. 2014

als

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Background: Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a pro-inflammatory cytokine with growth factor-like properties for monocytes and dendritic cells. Methods: Study subjects were recruited from the hospital in Hilla city. Healthy controls (n=15) and D.M. patients (n=35) were included in the study. Serum levels of GM-CSF and Anti-Insulin Antibody (AIA) measured by using ELISA technique. Results: The serum GM-CSF levels were significantly higher among diabetes subjects as compared with subjects without diabetes and results showed a high significant in serum AIA and glucose levels in patient as compare with control (p=0.009, P=0.001). The serum GM-CSF levels were increased in age group (45-54 years) shows the higher percent (42.85%) of patients with diabetes, with decreased of AIA and GM-CSF level rather than other age groups. Conclusions: There is indirect relationship between AIA and GM-CSF level and that is mean increased AIA and glucose level reflect the reduced GM-CSF level among the diabetic patients may be used as biomarker or use GM-CSF as co-therapy with insulin.

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GM-CSF- and M-CSF-dependent macrophage phenotypes display differential dependence on Type I interferon signaling

Cited by 254 publications

References 64 publications

Identification of a Unique Hybrid Macrophage-Polarization State following Recovery from Lipopolysaccharide Tolerance

Identification of a Unique Hybrid Macrophage-Polarization State following Recovery from Lipopolysaccharide Tolerance

TSC1 controls IL-1β expression in macrophages via mTORC1-dependent C/EBPβ pathway

Impact of Serum Granulocyte-Macrophage Colony-Stimulating Factor Levels among Diabetes Patients in Hilla City - Iraq

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