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Inhibition of TLR4 Induces M2 Microglial Polarization and Provides Neuroprotection via the NLRP3 Inflammasome in Alzheimer’s Disease

Cui, Weigang, Sun, Chunli, Ma, Yuqi, Wang, Songtao, Wang, Xianwei, Zhang, Yinghua·2020·Frontiers in Neuroscience
DOI 10.3389/fnins.2020.00444PMC PMC7251077
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FIGURE 1 TLR4 expressions were increased in the APP/PS1 Transgenic Mice. TLR4 levels in 6-month-old APP/PS1 transgenic and WT mice were shown by Western blot (A). Confocal analysis for Aβ (red) and TLR4 (green) revealed that Aβ deposition was surrounded by TLR4-positive cells in APP/PS1 transgenic AD mice (B). TLR4 (green) colocalized with CD11b (red) (C), which is indicated by an arrow. Scale bar: 20 μm. GAPDH was used as a loading control, and the densitometry was quantified. Data were analyzed with Student’s t-test. Data are expressed as mean ± SD, n = 5 for each group (∗∗P < 0.01 compared with the WT mice).
FIGURE 1 TLR4 expressions were increased in the APP/PS1 Transgenic Mice. TLR4 levels in 6-month-old APP/PS1 transgenic and WT mice were shown by Western blot (A). Confocal analysis for Aβ (red) and TLR4 (green) revealed that Aβ deposition was surrounded by TLR4-positive cells in APP/PS1 transgenic AD mice (B). TLR4 (green) colocalized with CD11b (red) (C), which is indicated by an arrow. Scale bar: 20 μm. GAPDH was used as a loading control, and the densitometry was quantified. Data were analyzed with Student’s t-test. Data are expressed as mean ± SD, n = 5 for each group (∗∗P < 0.01 compared with the WT mice).CC BY · PubMed Central
FIGURE 2 Microglial morphological changes in the PFC in APP/PS1 AD mice and its regulation by TAK-242 treatment. Representative immunofluorescence staining images show CD11b-positive microglia in the PFC of WT mice (A) and APP/PS1 transgenic mice (B). Morphological changes were suppressed by treatment with TAK-242, as shown in the immunofluorescence staining of vehicle (C) and TAK-242 (D) treatments. Hypertrophic morphology with thick microglial processes is indicated by an arrow. Panels (E) and (F) are magnifications of the rectangular region indicated in parts A and B, Scale bar: 5 μm. The area of CD11b positive reactivity is presented (G). The percentage of amoeboid microglial cells over the total microglial cells for each experimental group is presented (H). Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. Data are expressed as mean ± SD, n = 5 for each group (∗∗P < 0.01, ∗∗∗P < 0.001 compared with the WT mice group. ##P < 0.01 compared with the Vehicle-treated control group).
FIGURE 2 Microglial morphological changes in the PFC in APP/PS1 AD mice and its regulation by TAK-242 treatment. Representative immunofluorescence staining images show CD11b-positive microglia in the PFC of WT mice (A) and APP/PS1 transgenic mice (B). Morphological changes were suppressed by treatment with TAK-242, as shown in the immunofluorescence staining of vehicle (C) and TAK-242 (D) treatments. Hypertrophic morphology with thick microglial processes is indicated by an arrow. Panels (E) and (F) are magnifications of the rectangular region indicated in parts A and B, Scale bar: 5 μm. The area of CD11b positive reactivity is presented (G). The percentage of amoeboid microglial cells over the total microglial cells for each experimental group is presented (H). Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. Data are expressed as mean ± SD, n = 5 for each group (∗∗P < 0.01, ∗∗∗P < 0.001 compared with the WT mice group. ##P < 0.01 compared with the Vehicle-treated control group).CC BY · PubMed Central
FIGURE 3 M1- and M2-microglia associated markers and MyD88, NF-κB p65, and NLRP3 signaling were altered after TAK-242 treatment in APP/PS1 transgenic mice. ELISA analysis for the M1-microglia-associated markers iNOS and TNFα (A,B) and the M2-microglia-associated markers TREM-2 and Arg-1 (C,D). TAK-242 decreased the expression of MyD88, NF-κB p65, and NLRP3 (E–H). GAPDH was used as a loading control. Data were analyzed with Student’s t-test. Data are expressed as mean ± SD, n = 5 for each group (∗significant as compared with vehicle-treated control group, ∗∗P < 0.01, ∗∗∗P < 0.001).
FIGURE 3 M1- and M2-microglia associated markers and MyD88, NF-κB p65, and NLRP3 signaling were altered after TAK-242 treatment in APP/PS1 transgenic mice. ELISA analysis for the M1-microglia-associated markers iNOS and TNFα (A,B) and the M2-microglia-associated markers TREM-2 and Arg-1 (C,D). TAK-242 decreased the expression of MyD88, NF-κB p65, and NLRP3 (E–H). GAPDH was used as a loading control. Data were analyzed with Student’s t-test. Data are expressed as mean ± SD, n = 5 for each group (∗significant as compared with vehicle-treated control group, ∗∗P < 0.01, ∗∗∗P < 0.001).CC BY · PubMed Central
FIGURE 4 TLR4 inhibition treatment ameliorated impaired performance, decreased Aβ deposition, and exerted an anti-apoptosis effect in AD mice. The vehicle-treated group exhibited longer escape latencies to reach the hidden platform compared with TAK-242-treated mice (A), P < 0.05 by repeated-measure two-way ANOVA (Veh, n = 13; TAK-242, n = 13). The number of times of crossing the platform are shown (B), ∗∗P < 0.01 compared with the vehicle-treated group (Student’s t-test). No differences in the swim speeds or total distance (C,D) were found in TLR4 inhibition group compared with vehicle-treatment group. TAK-242 reduced the amyloid load in PFC and HC as the percentage of surface coverage (E,F), Scale bar 60 μm. TLR4 inhibition decreased the expression of Bax and the extent of DNA fragmentation (G–I), Data were analyzed with Student’s t-test. Data are expressed as mean ± SD. ∗∗P < 0.01, compared with vehicle-treated control.
FIGURE 4 TLR4 inhibition treatment ameliorated impaired performance, decreased Aβ deposition, and exerted an anti-apoptosis effect in AD mice. The vehicle-treated group exhibited longer escape latencies to reach the hidden platform compared with TAK-242-treated mice (A), P < 0.05 by repeated-measure two-way ANOVA (Veh, n = 13; TAK-242, n = 13). The number of times of crossing the platform are shown (B), ∗∗P < 0.01 compared with the vehicle-treated group (Student’s t-test). No differences in the swim speeds or total distance (C,D) were found in TLR4 inhibition group compared with vehicle-treatment group. TAK-242 reduced the amyloid load in PFC and HC as the percentage of surface coverage (E,F), Scale bar 60 μm. TLR4 inhibition decreased the expression of Bax and the extent of DNA fragmentation (G–I), Data were analyzed with Student’s t-test. Data are expressed as mean ± SD. ∗∗P < 0.01, compared with vehicle-treated control.CC BY · PubMed Central
FIGURE 5 TAK-242 regulated Aβ-induced M1 and M2 inflammatory microglia polarization. BV2 microglia were treated with various concentrations of TAK-242 for 24 h, and the cell viability was then measured by MTT assays (A). The optimal dose of TAK-242 in inhibiting Aβ-induced inflammation response was analyzed by ELISA assay (B). The expressions of iNOS, TNFα, TREM-2, and Arg-1 (C–F) were measured by ELISA kit. Data were analyzed with Student’s t-test or one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 compared with the Vehicle-treated control group. ##P < 0.01 compared with the Aβ25–35 (25 μM)-treated group).
FIGURE 5 TAK-242 regulated Aβ-induced M1 and M2 inflammatory microglia polarization. BV2 microglia were treated with various concentrations of TAK-242 for 24 h, and the cell viability was then measured by MTT assays (A). The optimal dose of TAK-242 in inhibiting Aβ-induced inflammation response was analyzed by ELISA assay (B). The expressions of iNOS, TNFα, TREM-2, and Arg-1 (C–F) were measured by ELISA kit. Data were analyzed with Student’s t-test or one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 compared with the Vehicle-treated control group. ##P < 0.01 compared with the Aβ25–35 (25 μM)-treated group).CC BY · PubMed Central
FIGURE 6 TAK-242 promoted microglial phagocytosis. The purity of the BV2 cell line was identified by immunostaining with an CD11b antibody specific to microglia (A–C). Scale bar: 20 μm. Compared with Aβ-treated control cells, the effect of TAK-242 on microglial phagocytosis was assessed by the number of fluorescent microbeads (yellow) in cells. CD11b-labeled microglia are shown in red, and DAPI-labeled cell nuclei are shown in blue. Fluorescent microbeads in yellow are indicated by an arrow (D,E). Scale bar: 20 μm. Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗∗∗P < 0.001 compared with the Vehicle treated group. ###P < 0.001 compared with the Aβ25–35 (25 μM)-treated group).
FIGURE 6 TAK-242 promoted microglial phagocytosis. The purity of the BV2 cell line was identified by immunostaining with an CD11b antibody specific to microglia (A–C). Scale bar: 20 μm. Compared with Aβ-treated control cells, the effect of TAK-242 on microglial phagocytosis was assessed by the number of fluorescent microbeads (yellow) in cells. CD11b-labeled microglia are shown in red, and DAPI-labeled cell nuclei are shown in blue. Fluorescent microbeads in yellow are indicated by an arrow (D,E). Scale bar: 20 μm. Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗∗∗P < 0.001 compared with the Vehicle treated group. ###P < 0.001 compared with the Aβ25–35 (25 μM)-treated group).CC BY · PubMed Central
FIGURE 7 TAK-242 suppressed Aβ-induced MyD88/NF-κB p65 and NLRP3 inflammasome activation and Aβ-induced apoptosis in BV2 microglial cells. TAK-242 suppressed the expression of MyD88 NF-κB p65 and NLRP3 by Western blot (A,B). TAK-242 treatment decreased the level of Bax and DNA fragmentation in SH-SY5Y cells (C,D) and in primary neuronal cells (E,F). GAPDH was used as a loading control. Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗∗P < 0.01, ∗∗∗P < 0.001 compared with the Vehicle treated group. ##P < 0.01, ###P < 0.001 compared with the Aβ25–35 (25 μM)-treated group).
FIGURE 7 TAK-242 suppressed Aβ-induced MyD88/NF-κB p65 and NLRP3 inflammasome activation and Aβ-induced apoptosis in BV2 microglial cells. TAK-242 suppressed the expression of MyD88 NF-κB p65 and NLRP3 by Western blot (A,B). TAK-242 treatment decreased the level of Bax and DNA fragmentation in SH-SY5Y cells (C,D) and in primary neuronal cells (E,F). GAPDH was used as a loading control. Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗∗P < 0.01, ∗∗∗P < 0.001 compared with the Vehicle treated group. ##P < 0.01, ###P < 0.001 compared with the Aβ25–35 (25 μM)-treated group).CC BY · PubMed Central
FIGURE 8 Effects of NLRP3 Gene Silencing on Aβ-Induced M1 and M2 inflammatory microglial polarization. (A,B) BV2 cells transfected with control or NLRP3-specific siRNA for 48 h. The relative levels of NLRP3 to GADPH protein expression were determined by Western blot. Knockdown of NLRP3 mRNA by NLRP3 siRNA in BV2 microglia significantly mitigated Aβ-induced levels on M1 markers (iNOS and TNFα) (C,D), and the Aβ-induced levels of iNOS and TNFα were also mitigated by TAK-242 treatment. Consistent with these findings, increases in TREM-2 and Arg-1 expressions were facilitated by treating siRNA-NLRP3 (E,F) in cultured supernatant, as measured by ELISA. Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗significant as compared with the vehicle-treated group, ∗∗∗P < 0.001. #significant as compared with the Aβ25-35 (25 μM)-treated group, #P < 0.05. $Significant as compared with the Aβ + siRNA NLRP3-treated group, $P < 0.05).
FIGURE 8 Effects of NLRP3 Gene Silencing on Aβ-Induced M1 and M2 inflammatory microglial polarization. (A,B) BV2 cells transfected with control or NLRP3-specific siRNA for 48 h. The relative levels of NLRP3 to GADPH protein expression were determined by Western blot. Knockdown of NLRP3 mRNA by NLRP3 siRNA in BV2 microglia significantly mitigated Aβ-induced levels on M1 markers (iNOS and TNFα) (C,D), and the Aβ-induced levels of iNOS and TNFα were also mitigated by TAK-242 treatment. Consistent with these findings, increases in TREM-2 and Arg-1 expressions were facilitated by treating siRNA-NLRP3 (E,F) in cultured supernatant, as measured by ELISA. Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗significant as compared with the vehicle-treated group, ∗∗∗P < 0.001. #significant as compared with the Aβ25-35 (25 μM)-treated group, #P < 0.05. $Significant as compared with the Aβ + siRNA NLRP3-treated group, $P < 0.05).CC BY · PubMed Central

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Metadata

Authors
Cui, W., Sun, C., Ma, Y., Wang, S., Wang, X., & Zhang, Y.
Venue
Frontiers in Neuroscience
Publisher
Frontiers Media SA
Published
2020-05-20
Volume
14
ISSN
1662-453X
DOI
10.3389/fnins.2020.00444
PMC
PMC7251077
Cited by
220
References
2
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • National Natural Science Foundation of China (U1804185, 81873459, U1804166)
  • Science and Technology Department of Henan Province (192102310346)

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