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Interferon regulatory factor 8/interferon consensus sequence binding protein is a critical transcription factor for the physiological phenotype of microglia

Horiuchi, Makoto, Wakayama, Kouji, Itoh, Aki, Kawai, Kumi, Pleasure, David, Ozato, Keiko, Itoh, Takayuki·2012·Journal of Neuroinflammation
DOI 10.1186/1742-2094-9-227PMC PMC3546867
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Figure 1 IRF8-deficient microglia colonized the CNS normally, but could not be identified by AIF1/IBA1 immunoreactivity. The spinal cords obtained from adult Irf8+/+ and Irf8-/- mice were immunolabeled for various microglial markers (A), and positive cells in the dorsal column at the Th1 spinal level were quantified (B). Microglia were reliably identified as CD11b and PU.1 double positive cells in both Irf8+/+ and Irf8-/- CNS tissues (pink arrows in far left panels in A). Note that few Irf8-/- microglia demonstrated detectable immunoreactivity for AIF1/IBA1. Scale bar: 100 μm. **P < 0.01. (C) 20 μm-thick z-stack confocal images of the microglia immunolabeled for CD11b (green) and PU.1 (red) in the dorsal columns at the Th1 spinal level. CD11b-positive microglial processes were much sparser in the dorsal column of Irf8-/- mice than those in Irf8+/+ mice, and processes of Irf8-/- microglia were thicker and less elaborated than those of Irf8+/+ microglia. PU.1-positive microglial nuclei are indicated by arrows, demonstrating that similar numbers of microglia are distributed in the Irf8+/+ and Irf8-/- spinal cords in contrast to the different density of the microglial processes. Scale bar: 100 μm.
Figure 1 IRF8-deficient microglia colonized the CNS normally, but could not be identified by AIF1/IBA1 immunoreactivity. The spinal cords obtained from adult Irf8+/+ and Irf8-/- mice were immunolabeled for various microglial markers (A), and positive cells in the dorsal column at the Th1 spinal level were quantified (B). Microglia were reliably identified as CD11b and PU.1 double positive cells in both Irf8+/+ and Irf8-/- CNS tissues (pink arrows in far left panels in A). Note that few Irf8-/- microglia demonstrated detectable immunoreactivity for AIF1/IBA1. Scale bar: 100 μm. **P < 0.01. (C) 20 μm-thick z-stack confocal images of the microglia immunolabeled for CD11b (green) and PU.1 (red) in the dorsal columns at the Th1 spinal level. CD11b-positive microglial processes were much sparser in the dorsal column of Irf8-/- mice than those in Irf8+/+ mice, and processes of Irf8-/- microglia were thicker and less elaborated than those of Irf8+/+ microglia. PU.1-positive microglial nuclei are indicated by arrows, demonstrating that similar numbers of microglia are distributed in the Irf8+/+ and Irf8-/- spinal cords in contrast to the different density of the microglial processes. Scale bar: 100 μm.CC BY · PubMed Central
Figure 2 Irf8-/- CNS tissues contain significantly less microglial processes than Irf8+/+ tissues. (A) Dorsal columns at the Th1 spinal level were immunolabeled for CD11b and PU.1, and inverted confocal fluorescence images of 12 μm-thick transverse sections are shown in monochrome. Only cross-sectional areas of the dorsal columns are shown. The location of each microglial nucleus positive for PU.1 is indicated by a circle to demonstrate similar distributions of microglia between the Irf8+/+ and Irf8-/- dorsal columns, which contrasts to lower densities of CD11b-positive microglial processes in Irf8-/- mice than in Irf8+/+ mice. (B) Similar difference was observed in the coronal sections of the corpus callosum. (C) The percentages of CD11b-positive areas in the whole cross-sectional area of the dorsal column were measured and compared quantitatively between Irf8-/- (closed bar) and Irf8+/+ mice (open bar). Three 3-month-old animals were used in each genotype. **P < 0.01. Scale bar: 100 μm.
Figure 2 Irf8-/- CNS tissues contain significantly less microglial processes than Irf8+/+ tissues. (A) Dorsal columns at the Th1 spinal level were immunolabeled for CD11b and PU.1, and inverted confocal fluorescence images of 12 μm-thick transverse sections are shown in monochrome. Only cross-sectional areas of the dorsal columns are shown. The location of each microglial nucleus positive for PU.1 is indicated by a circle to demonstrate similar distributions of microglia between the Irf8+/+ and Irf8-/- dorsal columns, which contrasts to lower densities of CD11b-positive microglial processes in Irf8-/- mice than in Irf8+/+ mice. (B) Similar difference was observed in the coronal sections of the corpus callosum. (C) The percentages of CD11b-positive areas in the whole cross-sectional area of the dorsal column were measured and compared quantitatively between Irf8-/- (closed bar) and Irf8+/+ mice (open bar). Three 3-month-old animals were used in each genotype. **P < 0.01. Scale bar: 100 μm.CC BY · PubMed Central
Figure 3 IRF8-deficient microglia in the mixed glial cultures exhibited a hyperproliferative phenotype in response to M-CSF and GM-CSF. A-I, Phase contrast images of mixed glial cultures from Irf8+/+ (A-C), Irf8+/- (D-F), and Irf8-/- (G-I) brain tissues. Cells were transferred to medium alone (control), medium supplemented with M-CSF (20 ng/ml) or GM-CSF (20 ng/ml) at 5 days in vitro, and then maintained in the same medium for another 4 days. Most microglia were seen as phase-bright round cells on the sheet of flat glial cells. Scale Bar: 50 μm. (J-K) Percentages of EdU-positive cells in total CD11b+ (J) or CD11b- (K) cells in the mixed glial cultures of the respective genotypes. Cells treated medium alone (cont), or medium supplemented with M-CSF (20 ng/ml) or GM-CSF (20 ng/ml) for 4 days were exposed to EdU at 6 hours prior to fixation, and double-stained for CD11b and EdU. **P < 0.01 and N.S indicates no significant difference in a comparison of the two groups indicated.
Figure 3 IRF8-deficient microglia in the mixed glial cultures exhibited a hyperproliferative phenotype in response to M-CSF and GM-CSF. A-I, Phase contrast images of mixed glial cultures from Irf8+/+ (A-C), Irf8+/- (D-F), and Irf8-/- (G-I) brain tissues. Cells were transferred to medium alone (control), medium supplemented with M-CSF (20 ng/ml) or GM-CSF (20 ng/ml) at 5 days in vitro, and then maintained in the same medium for another 4 days. Most microglia were seen as phase-bright round cells on the sheet of flat glial cells. Scale Bar: 50 μm. (J-K) Percentages of EdU-positive cells in total CD11b+ (J) or CD11b- (K) cells in the mixed glial cultures of the respective genotypes. Cells treated medium alone (cont), or medium supplemented with M-CSF (20 ng/ml) or GM-CSF (20 ng/ml) for 4 days were exposed to EdU at 6 hours prior to fixation, and double-stained for CD11b and EdU. **P < 0.01 and N.S indicates no significant difference in a comparison of the two groups indicated.CC BY · PubMed Central
Figure 4 F4/80, CD11c, and Ly-6G expression in Irf8+/+ and Irf8-/- microglia in the mixed glial cultures maintained in the presence of M-CSF or GM-CSF. Mixed glial cells were cultured in medium alone (control) or medium supplemented with M-CSF (20 ng/ml) or GM-CSF (20 ng/ml) for 4 days, and labeled with anti-CD45 and anti-CD11b antibodies in combination with each of anti-F4/80, anti-CD11c or anti-Ly-6G antibodies. The bivariate plots show expression of CD11b, F4/80, CD11c and Ly-6G on gated CD45-positive cells. The quadrants were set using corresponding isotype controls.
Figure 4 F4/80, CD11c, and Ly-6G expression in Irf8+/+ and Irf8-/- microglia in the mixed glial cultures maintained in the presence of M-CSF or GM-CSF. Mixed glial cells were cultured in medium alone (control) or medium supplemented with M-CSF (20 ng/ml) or GM-CSF (20 ng/ml) for 4 days, and labeled with anti-CD45 and anti-CD11b antibodies in combination with each of anti-F4/80, anti-CD11c or anti-Ly-6G antibodies. The bivariate plots show expression of CD11b, F4/80, CD11c and Ly-6G on gated CD45-positive cells. The quadrants were set using corresponding isotype controls.CC BY · PubMed Central
Figure 5 Purified Irf8+/+ and Irf8-/- microglia in vitro. (A-D) Representative phase contrast (A, B) and immunocytochemical (C, D) pictures of the microglia isolated from the Irf8+/+ (A, C) and Irf8-/- (B, D) mixed glial cultures grown in the presence of M-CSF (20 ng/ml) by magnetic-activated cell sorting. Purified cells were immunolabeled for CD11b (green in C, D) at 24 h after isolation. Nuclei were counterstained with DAPI (blue). Scale Bar: 50 μm. (E)IRF8 and PU.1/SFPI1 mRNA levels in the purified Irf8+/+ microglia. Purified microglia were incubated in medium alone (control) or in the presence of IFNγ (IFNG, 100 ng/ml), lipopolysaccharide (LPS, 100 ng/ml) or both for 24 h. Reverse transcribed IRF8 and PU.1/SFPI1 cDNA levels are plotted as ratios to copy numbers of β-actin cDNA on a logarithmic scale. (F) Immunoblots for IRF8 confirmed the results of mRNA. (G) Purified Irf8-/- CD11b+ microglia were less proliferative than Irf8+/+ CD11b+ microglia even in the presence of exogenous M-CSF. Purified microglia were preincubated with medium alone for 24 h after isolation from Irf8+/+ (open bars) and Irf8-/- (closed bars) mixed glial cultures, and then treated with medium alone (control), or medium supplemented with M-CSF (20 ng/ml) or GM-CSF (20 ng/ml) for 24 h. After a 6 hour incubation with EdU, EdU-positive and DAPI-positive nuclei were counted. **P < 0.01 in comparison with control or between the two groups indicated.
Figure 5 Purified Irf8+/+ and Irf8-/- microglia in vitro. (A-D) Representative phase contrast (A, B) and immunocytochemical (C, D) pictures of the microglia isolated from the Irf8+/+ (A, C) and Irf8-/- (B, D) mixed glial cultures grown in the presence of M-CSF (20 ng/ml) by magnetic-activated cell sorting. Purified cells were immunolabeled for CD11b (green in C, D) at 24 h after isolation. Nuclei were counterstained with DAPI (blue). Scale Bar: 50 μm. (E)IRF8 and PU.1/SFPI1 mRNA levels in the purified Irf8+/+ microglia. Purified microglia were incubated in medium alone (control) or in the presence of IFNγ (IFNG, 100 ng/ml), lipopolysaccharide (LPS, 100 ng/ml) or both for 24 h. Reverse transcribed IRF8 and PU.1/SFPI1 cDNA levels are plotted as ratios to copy numbers of β-actin cDNA on a logarithmic scale. (F) Immunoblots for IRF8 confirmed the results of mRNA. (G) Purified Irf8-/- CD11b+ microglia were less proliferative than Irf8+/+ CD11b+ microglia even in the presence of exogenous M-CSF. Purified microglia were preincubated with medium alone for 24 h after isolation from Irf8+/+ (open bars) and Irf8-/- (closed bars) mixed glial cultures, and then treated with medium alone (control), or medium supplemented with M-CSF (20 ng/ml) or GM-CSF (20 ng/ml) for 24 h. After a 6 hour incubation with EdU, EdU-positive and DAPI-positive nuclei were counted. **P < 0.01 in comparison with control or between the two groups indicated.CC BY · PubMed Central
Figure 6 IRF8-deficient microglia demonstrated a reduced phagocytic capacity in vitro. Microglia from Irf8+/+ (A) and Irf8-/- (B) mice were incubated with Alexa Fluor™ 488-conjugated zymosan particles for 24 hours. Scale bar: 50 μm. (C-D) Percentages of Alexa Fluor™ 488-positive cells in total cells (C) and mean fluorescent intensity (MFI) of Alexa Fluor™ 488-positive cells (D) were measured in Irf8+/+, Irf8+/-, and Irf8-/- microglial cultures at 0, 1, 6, and 24 hour after adding the zymosan particles. The MFI of a non-phagocytosed Alexa Fluor™ 488-conjugated zymosan particle is also shown (Zymosan- Alexa488) in D. **P < 0.001 in comparison with the two groups indicated.
Figure 6 IRF8-deficient microglia demonstrated a reduced phagocytic capacity in vitro. Microglia from Irf8+/+ (A) and Irf8-/- (B) mice were incubated with Alexa Fluor™ 488-conjugated zymosan particles for 24 hours. Scale bar: 50 μm. (C-D) Percentages of Alexa Fluor™ 488-positive cells in total cells (C) and mean fluorescent intensity (MFI) of Alexa Fluor™ 488-positive cells (D) were measured in Irf8+/+, Irf8+/-, and Irf8-/- microglial cultures at 0, 1, 6, and 24 hour after adding the zymosan particles. The MFI of a non-phagocytosed Alexa Fluor™ 488-conjugated zymosan particle is also shown (Zymosan- Alexa488) in D. **P < 0.001 in comparison with the two groups indicated.CC BY · PubMed Central
Figure 7 AIF1/IBA1 expression in Irf8-/- microglia was reduced but still inducible by IFNγ. (A) Quantitative and kinetic analysis of AIF1/IBA1 mRNA in Irf8+/+ and Irf8-/- microglia after addition of medium alone (Control, open circle), IFNγ (IFNG, 100 ng/ml, closed circle), lipopolysaccharide (LPS, 100 ng/ml, open square) or both (closed square). Reverse transcribed cDNA levels at the indicated time points were quantified by qPCR and are plotted as ratios to copy numbers of β-actin cDNA on a logarithmic scale. Data were from at least three independent experiments. At time 0, data from controls are only shown. (B) Irf8-/- microglia expressed far less AIF1/IBA1 protein than Irf8+/+ microglia. Purified microglia were maintained in the medium containing IFNγ (IFNG, 100 ng/ml), lipopolysaccharide (LPS, 100 ng/ml) or both for 24 h. Subsequent immunoblots for β-actin (ACTB) are shown for equal protein loading.
Figure 7 AIF1/IBA1 expression in Irf8-/- microglia was reduced but still inducible by IFNγ. (A) Quantitative and kinetic analysis of AIF1/IBA1 mRNA in Irf8+/+ and Irf8-/- microglia after addition of medium alone (Control, open circle), IFNγ (IFNG, 100 ng/ml, closed circle), lipopolysaccharide (LPS, 100 ng/ml, open square) or both (closed square). Reverse transcribed cDNA levels at the indicated time points were quantified by qPCR and are plotted as ratios to copy numbers of β-actin cDNA on a logarithmic scale. Data were from at least three independent experiments. At time 0, data from controls are only shown. (B) Irf8-/- microglia expressed far less AIF1/IBA1 protein than Irf8+/+ microglia. Purified microglia were maintained in the medium containing IFNγ (IFNG, 100 ng/ml), lipopolysaccharide (LPS, 100 ng/ml) or both for 24 h. Subsequent immunoblots for β-actin (ACTB) are shown for equal protein loading.CC BY · PubMed Central
Figure 8 Kinetics of IFNB1 (A) and IL12B (B) mRNA levels in Irf8+/+ and Irf8-/- microglia after the exposure to IFNγ and lipopolysaccharide. Purified microglia were incubated in medium alone (Control, closed and open circle in the left panels) or in the presence of IFNγ (IFNG, 100 ng/ml), lipopolysaccharide (LPS, 100 ng/ml) or both (IFNG + LPS) for 24 h. IFNB1 and IL12B mRNA at the indicated time points were quantified by qPCR and are plotted as ratios to copy numbers of β-actin cDNA on a logarithmic scale. Data were calculated from at least three independent experiments in each genotype. At time 0, data from controls are only shown. **P < 0.01 and *P < 0.05, in a comparison of the two genotypes at the indicated time points.
Figure 8 Kinetics of IFNB1 (A) and IL12B (B) mRNA levels in Irf8+/+ and Irf8-/- microglia after the exposure to IFNγ and lipopolysaccharide. Purified microglia were incubated in medium alone (Control, closed and open circle in the left panels) or in the presence of IFNγ (IFNG, 100 ng/ml), lipopolysaccharide (LPS, 100 ng/ml) or both (IFNG + LPS) for 24 h. IFNB1 and IL12B mRNA at the indicated time points were quantified by qPCR and are plotted as ratios to copy numbers of β-actin cDNA on a logarithmic scale. Data were calculated from at least three independent experiments in each genotype. At time 0, data from controls are only shown. **P < 0.01 and *P < 0.05, in a comparison of the two genotypes at the indicated time points.CC BY · PubMed Central
Figure 9 A defective phenotype of IRF8-deficient microglia in vivo in the cuprizone-induced demyelination model. (A) There was no quantitative difference in corpus callosal microglia, myelinating oligodendrocytes, and NG2-positive oligodendroglial precursor cells between Irf8+/+ and Irf8-/- mice before cuprizone feeding. Microglia and myelinating oligodendrocytes were identified by immunoreactivity for nuclear PU.1 and for the cytosolic CC1 epitope, respectively. (B) Cuprizone-mediated demyelination in the medial corpus callosum in Irf8+/+ and Irf8-/- mice. Representative LFB-PAS-stained paraffin sections of the medial corpus callosi of Irf8+/+ and Irf8-/- mice at 4 and 6 weeks of cuprizone diet (left panel). Scale bar: 100 μm. Reduction of myelinating oligodendrocytes in the corpus callosum. CC1+ oligodendrocytes per unit area of 6 μm-thick coronal sections were counted. At least three mice were used for each data point (right graph). (C) Microglial accumulation in the corpus callosum was delayed in Irf8-/- mice compared with Irf8+/+ mice. CD11b+ microglia with PU.1+ nuclei were quantified in 6 μm-thick coronal sections as in B (right graph). Note that the abnormal oval cell shape of activated Irf8-/- microglia at 6 weeks of cuprizone feeding. Scale bar: 100 μm. (D) Oil red O plus hematoxylin staining of the corpus callosum of Irf8+/+ and Irf8-/- mice at 0, 4 and 6 weeks of cuprizone feeding. Lipid-rich myelin debris visualized by Oil red O staining (red arrows) rapidly accumulated in the corpus callosum of Irf8-/- mice, as demyelination progressed. Scale bar: 25 μm. Data are presented as mean ± standard error. *P < 0.05 by Mann-Whitney U test.
Figure 9 A defective phenotype of IRF8-deficient microglia in vivo in the cuprizone-induced demyelination model. (A) There was no quantitative difference in corpus callosal microglia, myelinating oligodendrocytes, and NG2-positive oligodendroglial precursor cells between Irf8+/+ and Irf8-/- mice before cuprizone feeding. Microglia and myelinating oligodendrocytes were identified by immunoreactivity for nuclear PU.1 and for the cytosolic CC1 epitope, respectively. (B) Cuprizone-mediated demyelination in the medial corpus callosum in Irf8+/+ and Irf8-/- mice. Representative LFB-PAS-stained paraffin sections of the medial corpus callosi of Irf8+/+ and Irf8-/- mice at 4 and 6 weeks of cuprizone diet (left panel). Scale bar: 100 μm. Reduction of myelinating oligodendrocytes in the corpus callosum. CC1+ oligodendrocytes per unit area of 6 μm-thick coronal sections were counted. At least three mice were used for each data point (right graph). (C) Microglial accumulation in the corpus callosum was delayed in Irf8-/- mice compared with Irf8+/+ mice. CD11b+ microglia with PU.1+ nuclei were quantified in 6 μm-thick coronal sections as in B (right graph). Note that the abnormal oval cell shape of activated Irf8-/- microglia at 6 weeks of cuprizone feeding. Scale bar: 100 μm. (D) Oil red O plus hematoxylin staining of the corpus callosum of Irf8+/+ and Irf8-/- mice at 0, 4 and 6 weeks of cuprizone feeding. Lipid-rich myelin debris visualized by Oil red O staining (red arrows) rapidly accumulated in the corpus callosum of Irf8-/- mice, as demyelination progressed. Scale bar: 25 μm. Data are presented as mean ± standard error. *P < 0.05 by Mann-Whitney U test.CC BY · PubMed Central

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Metadata

Authors
Horiuchi, M., Wakayama, K., Itoh, A., Kawai, K., Pleasure, D., Ozato, K., & Itoh, T.
Venue
Journal of Neuroinflammation
Publisher
Springer Science and Business Media LLC
Published
2012-09-28
Volume
9
Issue
1
ISSN
1742-2094
DOI
10.1186/1742-2094-9-227
PMC
PMC3546867
Cited by
65
References
15
Language
en
Licence
www.creativecommons.org/licenses/by/2.0 (unspecified)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

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