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Abrogated Inflammatory Response Promotes Neurogenesis in a Murine Model of Japanese Encephalitis

Das, Sulagna, Dutta, Kallol, Kumawat, Kanhaiya Lal, Ghoshal, Ayan, Adhya, Dwaipayan, Basu, Anirban·2011·PLoS ONE
DOI 10.1371/journal.pone.0017225PMC PMC3048396
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Figure 1 Decreased production of proinflammatory cyto/chemokines across various regions of the adult JEV-infected brain by minocycline administration. Protein isolated from cortex, hippocampus, SVZ and striatum of Control, JEV-infected and JEV+M animals were analyzed using CBA. The graphs depict the fold increase in TNF-α (A), IFN-γ (B), IL-6 (C) and MCP-1 (D) levels in the JEV-infected and JEV+M treated brain areas compared to those from control brain. A profound increase in the cytokine level of TNF-α (A), IFN-γ (B), IL-6 (C), and MCP-1 (D) was observed in all the areas of JEV-infected brain, which was dramatically reduced upon minocycline administration in JEV+M animals. (Values represent means ± SEM from five animals in each group; * significant change from JEV, p<0.01).
Figure 1 Decreased production of proinflammatory cyto/chemokines across various regions of the adult JEV-infected brain by minocycline administration. Protein isolated from cortex, hippocampus, SVZ and striatum of Control, JEV-infected and JEV+M animals were analyzed using CBA. The graphs depict the fold increase in TNF-α (A), IFN-γ (B), IL-6 (C) and MCP-1 (D) levels in the JEV-infected and JEV+M treated brain areas compared to those from control brain. A profound increase in the cytokine level of TNF-α (A), IFN-γ (B), IL-6 (C), and MCP-1 (D) was observed in all the areas of JEV-infected brain, which was dramatically reduced upon minocycline administration in JEV+M animals. (Values represent means ± SEM from five animals in each group; * significant change from JEV, p<0.01).CC BY · PubMed Central
Figure 2 Attenuation of inflammatory milieu in the infected adult SVZ by minocycline administration. Cryostat sections of brains from control, JEV and JEV+M animal groups were stained for cells of monocyte/macrophage lineage (CD11b), T-cells (CD3) and neutrophils (Ly6/C), (FITC, green) (A). Images were acquired using oil immersion lens of confocal microscope. These peripheral immune cells were completely absent in the SVZ of control and JEV+M brains. In SVZ of JEV-infected animals, a large number of these cells were observed; scale bar is 50 µ. Protein isolated from SVZ of control, JEV and JEV+M animals were analyzed by immunoblot (B). Increased expression of iNOS and Cox-2 in JEV-infected SVZ was reduced significantly in JEV+M SVZ. The graphs represent densitometric quantification of proteins bands of iNOS and Cox-2 normalised to β-actin (C). Values represent the means ± SEM from five animals in each group (* significant change from control p<0.01; # significant change from JEV-infected samples p<0.01).
Figure 2 Attenuation of inflammatory milieu in the infected adult SVZ by minocycline administration. Cryostat sections of brains from control, JEV and JEV+M animal groups were stained for cells of monocyte/macrophage lineage (CD11b), T-cells (CD3) and neutrophils (Ly6/C), (FITC, green) (A). Images were acquired using oil immersion lens of confocal microscope. These peripheral immune cells were completely absent in the SVZ of control and JEV+M brains. In SVZ of JEV-infected animals, a large number of these cells were observed; scale bar is 50 µ. Protein isolated from SVZ of control, JEV and JEV+M animals were analyzed by immunoblot (B). Increased expression of iNOS and Cox-2 in JEV-infected SVZ was reduced significantly in JEV+M SVZ. The graphs represent densitometric quantification of proteins bands of iNOS and Cox-2 normalised to β-actin (C). Values represent the means ± SEM from five animals in each group (* significant change from control p<0.01; # significant change from JEV-infected samples p<0.01).CC BY · PubMed Central
Figure 3 Replenishment of proliferating cells in the infected adult SVZ by minocycline administration. Cryostat sections of brains from control, control+M, JEV and JEV+M animal groups were stained for markers of proliferation- Ki-67 (A) and PCNA (B) and developed using DAB substrate. BrdU was also administered to animals for 5 days at 50 mg/kg body weight and then animals were sacrificed 6 h after the last BrdU injection. Cryostat sections from BrdU administered animals from all groups were stained using anti-BrdU antibody (C). Discrete population of cells in control SVZ show localisation of all the antigens. While reduced population of all three cell types were observed in JEV-infected SVZ, however, they were replenished in the SVZ from JEV+M animals. The graphs represent the number of Ki-67 (D), PCNA (E) and BrdU (F) positive cells in the SVZ from the different treatment groups. Cell counting was done using5 serial sections from 3 animals with Leica IM50 software. Values represent means ± SEM from three animals in each group (* significant change from control, p<0.05; #significant change from JEV-infected animals, p<0.05); scale bar is 50 µ.
Figure 3 Replenishment of proliferating cells in the infected adult SVZ by minocycline administration. Cryostat sections of brains from control, control+M, JEV and JEV+M animal groups were stained for markers of proliferation- Ki-67 (A) and PCNA (B) and developed using DAB substrate. BrdU was also administered to animals for 5 days at 50 mg/kg body weight and then animals were sacrificed 6 h after the last BrdU injection. Cryostat sections from BrdU administered animals from all groups were stained using anti-BrdU antibody (C). Discrete population of cells in control SVZ show localisation of all the antigens. While reduced population of all three cell types were observed in JEV-infected SVZ, however, they were replenished in the SVZ from JEV+M animals. The graphs represent the number of Ki-67 (D), PCNA (E) and BrdU (F) positive cells in the SVZ from the different treatment groups. Cell counting was done using5 serial sections from 3 animals with Leica IM50 software. Values represent means ± SEM from three animals in each group (* significant change from control, p<0.05; #significant change from JEV-infected animals, p<0.05); scale bar is 50 µ.CC BY · PubMed Central
Figure 4 Population of migrating neuroblasts restored in adult infected SVZ by minocycline administration. Cryostat sections of brains from control, JEV and JEV+M animal groups were labelled for proliferating cells of neuronal lineage (BrdU+DCX double staining) (A) or for migrating neuroblasts (DCX positive cells) (B). Control SVZ show marked co-localization of BrdU (Alexa Fluor, red) and DCX (FITC, green). These double positive cells were distinctly lesser in the JEV-infected SVZ compared to control SVZ, which was however restored in JEV+M SVZ (A). DCX staining (FITC, green) show migrating neuroblasts in control SVZ and in SVZ from JEV+M animals with neurite extending outwards (shown by arrowheads), was completely absent in JEV-infected SVZ (B); scale bar is 50 µ. Protein isolated from SVZ of control, JEV and JEV+M animals were analyzed by immunoblot (C). Expression of DCX, PSD-95 and PCNA declined in JEV-infected SVZ, which in JEV+M SVZ was elevated almost to control levels. The graph represents densitometric quantification of proteins bands of DCX, PSD-95 and PCNA, normalised to β-actin (D). Values represent the means ± SEM from five animals in each group (* significant change from control p<0.05; # significant change from JEV samples p<0.05).
Figure 4 Population of migrating neuroblasts restored in adult infected SVZ by minocycline administration. Cryostat sections of brains from control, JEV and JEV+M animal groups were labelled for proliferating cells of neuronal lineage (BrdU+DCX double staining) (A) or for migrating neuroblasts (DCX positive cells) (B). Control SVZ show marked co-localization of BrdU (Alexa Fluor, red) and DCX (FITC, green). These double positive cells were distinctly lesser in the JEV-infected SVZ compared to control SVZ, which was however restored in JEV+M SVZ (A). DCX staining (FITC, green) show migrating neuroblasts in control SVZ and in SVZ from JEV+M animals with neurite extending outwards (shown by arrowheads), was completely absent in JEV-infected SVZ (B); scale bar is 50 µ. Protein isolated from SVZ of control, JEV and JEV+M animals were analyzed by immunoblot (C). Expression of DCX, PSD-95 and PCNA declined in JEV-infected SVZ, which in JEV+M SVZ was elevated almost to control levels. The graph represents densitometric quantification of proteins bands of DCX, PSD-95 and PCNA, normalised to β-actin (D). Values represent the means ± SEM from five animals in each group (* significant change from control p<0.05; # significant change from JEV samples p<0.05).CC BY · PubMed Central
Figure 5 Expression of inflammatory molecules in JEV activated BV2 is attenuated by minocycline treatment. Mouse microglia BV2 were either control (C), JEV-infected (JEV) or JEV-infected and treated with minocycline (JEV+M). After 6 h of minocycline treatment p.i., fresh DMEM-F12 media was added to all conditions. After additional 6 h, CM from BV2 cells from all conditions was collected for CBA and protein extracted for immunoblot. The graphs depict the concentration in pg/ml of cyto/chemokines TNF-α (A), IL-6 (B) and MCP-1 (C) in Control, JEV-infected and JEV+M treated BV2 cells. Values represent means ± SEM from 3 independent experiments performed in duplicate (* significant change from control, p<0.05; # significant change from JEV, p<0.05). Protein isolated from BV2 cells from C, JEV and JEV+M conditions were analyzed by immunoblot (D). The graphs represent the densitometric quantification of protein bands- iNOS and Cox-2 normalised to β-actin (E). Values represent mean ± SEM from 3 independent experiments performed in duplicate (* significant change from control, p<0.05; # significant change from JEV, p<0.05).
Figure 5 Expression of inflammatory molecules in JEV activated BV2 is attenuated by minocycline treatment. Mouse microglia BV2 were either control (C), JEV-infected (JEV) or JEV-infected and treated with minocycline (JEV+M). After 6 h of minocycline treatment p.i., fresh DMEM-F12 media was added to all conditions. After additional 6 h, CM from BV2 cells from all conditions was collected for CBA and protein extracted for immunoblot. The graphs depict the concentration in pg/ml of cyto/chemokines TNF-α (A), IL-6 (B) and MCP-1 (C) in Control, JEV-infected and JEV+M treated BV2 cells. Values represent means ± SEM from 3 independent experiments performed in duplicate (* significant change from control, p<0.05; # significant change from JEV, p<0.05). Protein isolated from BV2 cells from C, JEV and JEV+M conditions were analyzed by immunoblot (D). The graphs represent the densitometric quantification of protein bands- iNOS and Cox-2 normalised to β-actin (E). Values represent mean ± SEM from 3 independent experiments performed in duplicate (* significant change from control, p<0.05; # significant change from JEV, p<0.05).CC BY · PubMed Central
Figure 6 Impaired neurosphere formation by soluble mediators from JEV activated microglia is reversed by minocycline treatment. Single cell suspensions of NSPCs were cultured alone (C) or in presence of BV2-derived CM under 3 conditions- BV2(C), BV2(JEV), BV2(JEV+M) for 3 days. Phase-contrast micrographs of neurospheres were acquired under 10× magnification (A). Scale bar is 100 µ. The number of neurospheres was counted from 10 different fields for each condition and the average diameter of the spheres was measured using Leica IM50 software. The graphs represent the average number of spheres (B) and their average diameter in microns (C). The numbers of colony forming neurospheres do not show any significant difference between groups (B). The reduction in size of neurospheres grown in CM from BV2(JEV) was prominent compared to CM-BV2(C) or CM-BV2(JEV+M) conditions (C). Values represent mean ± SEM from 3 independent experiments performed in duplicate (** significant change from control, p<0.05; * significant change from CM-BV2(C), p<0.01; # significant change from CM-BV2(JEV), p<0.01).
Figure 6 Impaired neurosphere formation by soluble mediators from JEV activated microglia is reversed by minocycline treatment. Single cell suspensions of NSPCs were cultured alone (C) or in presence of BV2-derived CM under 3 conditions- BV2(C), BV2(JEV), BV2(JEV+M) for 3 days. Phase-contrast micrographs of neurospheres were acquired under 10× magnification (A). Scale bar is 100 µ. The number of neurospheres was counted from 10 different fields for each condition and the average diameter of the spheres was measured using Leica IM50 software. The graphs represent the average number of spheres (B) and their average diameter in microns (C). The numbers of colony forming neurospheres do not show any significant difference between groups (B). The reduction in size of neurospheres grown in CM from BV2(JEV) was prominent compared to CM-BV2(C) or CM-BV2(JEV+M) conditions (C). Values represent mean ± SEM from 3 independent experiments performed in duplicate (** significant change from control, p<0.05; * significant change from CM-BV2(C), p<0.01; # significant change from CM-BV2(JEV), p<0.01).CC BY · PubMed Central
Figure 7 Induction of cell cycle arrest by soluble mediators from JEV activated microglia is reversed by minocycline treatment. Cell cycle analysis of single cell suspensions of neurospheres grown alone or in presence of BV2-CM was performed using RNase/PI buffer and detected by FACS. Gates were set to assess the percentages of G0/G1 (2n DNA), S (>2n DNA) and G2/M (4n DNA) cells using Cell Quest Pro Software, and the representative histograms have been shown (A). Data is representative of 3 independent experiments. Protein isolated from control and BV2-CM treated neurospheres were immunoblotted for checkpoint proteins p21, p27, p53 and p107 (B). The expression of all these proteins increased in neurospheres grown in CM from BV2(JEV) compared to that from BV2(C) or from BV2(JEV+M) (C). Densitometric analysis of immunoblot normalised to β-actin was plotted as a bar graph. Values represent mean ± SEM from three independent experiments. (** significant change from control, p<0.05; * significant change from CM-BV2(C), p<0.05; # significant change from CM-BV2(JEV), p<0.05).
Figure 7 Induction of cell cycle arrest by soluble mediators from JEV activated microglia is reversed by minocycline treatment. Cell cycle analysis of single cell suspensions of neurospheres grown alone or in presence of BV2-CM was performed using RNase/PI buffer and detected by FACS. Gates were set to assess the percentages of G0/G1 (2n DNA), S (>2n DNA) and G2/M (4n DNA) cells using Cell Quest Pro Software, and the representative histograms have been shown (A). Data is representative of 3 independent experiments. Protein isolated from control and BV2-CM treated neurospheres were immunoblotted for checkpoint proteins p21, p27, p53 and p107 (B). The expression of all these proteins increased in neurospheres grown in CM from BV2(JEV) compared to that from BV2(C) or from BV2(JEV+M) (C). Densitometric analysis of immunoblot normalised to β-actin was plotted as a bar graph. Values represent mean ± SEM from three independent experiments. (** significant change from control, p<0.05; * significant change from CM-BV2(C), p<0.05; # significant change from CM-BV2(JEV), p<0.05).CC BY · PubMed Central
Figure 8 Decreased neuronal differentiation of NSPCs by soluble mediators from JEV activated microglia is reversed by minocycline treatment. Phase contrast micrographs of differentiating neurospheres from control and BV2 derived CM treated NSPCs 2 days after induction of differentiation on PDL-coated plates (A). Impaired migration and differentiation of cells from the periphery of the spheres is observed in CM-BV2(JEV) conditions. Control and BV2-Cm treated neurospheres were dissociated and single cell suspensions of NSPCs were differentiated for 2 days. The cells were fixed and double immunocytochemistry for β-III tubulin (neuronal phenotype) and GFAP (astrocytic phenotype) was performed and mounted with Vectashield containing DAPI. Distinct β-III tubulin positive cells (FITC, green) and GFAP positive cells (Alexa 594, red) were observed, indicating NSPCs undergoing differentiation (B). The percentage of β-III tubulin positive cells were calculated from 5 different fields and plotted as a representative graph (C). RNA was isolated from these NSPCs after 2 days of differentiation and qRT-PCR was performed for β-III tubulin expression. The graph represents relative mRNA expression of β-III tubulin normalised to the expression of constitutive 18S rRNA (D). Values represent mean ± SEM from three independent experiments performed in duplicate. (** significant change from control, p<0.05; * significant change from CM-BV2(C), p<0.01; # significant change from CM-BV2(JEV), p<0.01). Scale bar corresponds to 50 microns.
Figure 8 Decreased neuronal differentiation of NSPCs by soluble mediators from JEV activated microglia is reversed by minocycline treatment. Phase contrast micrographs of differentiating neurospheres from control and BV2 derived CM treated NSPCs 2 days after induction of differentiation on PDL-coated plates (A). Impaired migration and differentiation of cells from the periphery of the spheres is observed in CM-BV2(JEV) conditions. Control and BV2-Cm treated neurospheres were dissociated and single cell suspensions of NSPCs were differentiated for 2 days. The cells were fixed and double immunocytochemistry for β-III tubulin (neuronal phenotype) and GFAP (astrocytic phenotype) was performed and mounted with Vectashield containing DAPI. Distinct β-III tubulin positive cells (FITC, green) and GFAP positive cells (Alexa 594, red) were observed, indicating NSPCs undergoing differentiation (B). The percentage of β-III tubulin positive cells were calculated from 5 different fields and plotted as a representative graph (C). RNA was isolated from these NSPCs after 2 days of differentiation and qRT-PCR was performed for β-III tubulin expression. The graph represents relative mRNA expression of β-III tubulin normalised to the expression of constitutive 18S rRNA (D). Values represent mean ± SEM from three independent experiments performed in duplicate. (** significant change from control, p<0.05; * significant change from CM-BV2(C), p<0.01; # significant change from CM-BV2(JEV), p<0.01). Scale bar corresponds to 50 microns.CC BY · PubMed Central

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Metadata

Authors
Das, S., Dutta, K., Kumawat, K. L., Ghoshal, A., Adhya, D., & Basu, A.
Venue
PLoS ONE
Publisher
Public Library of Science (PLoS)
Published
2011-03-03
Volume
6
Issue
3
Pages
e17225
ISSN
1932-6203
DOI
10.1371/journal.pone.0017225
PMC
PMC3048396
Cited by
65
References
8
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (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.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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