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cd36 receptor blocking antibody  (Biophotonic Solutions Inc)

 
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    Biophotonic Solutions Inc cd36 receptor blocking antibody
    Real-time bioluminescence imaging of theTLR2 signals after LPS challenge. ( a ) Schematic presentation of experimental protocol used for the treatment with <t>anti-CD36</t> antibodies in P8-P9 mice. ( b – j ) Representative images of the bioluminescent signals recorded from the brains of living P10–P12 TLR2-luc-GFP mice treated with anti-CD36 antibody ( b – d ), LPS ( e – g ) or pre-treated with anti-CD36 antibody followed by systemic LPS injection ( h – j ). Note that a robust TLR2 induction 24 h post-LPS treatment is significantly reduced when the pups are pre-treated with anti-CD36. The scales on the right are the colour maps for source intensity. The scale ranges differ at individual ages. ( k ) Quantification of the in vivo bioluminescence data from P8–P12 (in photons per second, p/s). One way ANOVA (anti-CD36 vs LPS *p ≤ 0.05, LPS vs anti-CD36 + LPS *p ≤ 0.05).
    Cd36 Receptor Blocking Antibody, supplied by Biophotonic Solutions Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cd36+receptor+blocking+antibody/pmc09911392-41-4-11?v=Biophotonic+Solutions+Inc
    Average 90 stars, based on 1 article reviews
    cd36 receptor blocking antibody - by Bioz Stars, 2026-08
    90/100 stars

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    1) Product Images from "CD36 neutralisation blunts TLR2-IRF7 but not IRF3 pathway in neonatal mouse brain and immature human microglia following innate immune challenge"

    Article Title: CD36 neutralisation blunts TLR2-IRF7 but not IRF3 pathway in neonatal mouse brain and immature human microglia following innate immune challenge

    Journal: Scientific Reports

    doi: 10.1038/s41598-023-29423-0

    Real-time bioluminescence imaging of theTLR2 signals after LPS challenge. ( a ) Schematic presentation of experimental protocol used for the treatment with anti-CD36 antibodies in P8-P9 mice. ( b – j ) Representative images of the bioluminescent signals recorded from the brains of living P10–P12 TLR2-luc-GFP mice treated with anti-CD36 antibody ( b – d ), LPS ( e – g ) or pre-treated with anti-CD36 antibody followed by systemic LPS injection ( h – j ). Note that a robust TLR2 induction 24 h post-LPS treatment is significantly reduced when the pups are pre-treated with anti-CD36. The scales on the right are the colour maps for source intensity. The scale ranges differ at individual ages. ( k ) Quantification of the in vivo bioluminescence data from P8–P12 (in photons per second, p/s). One way ANOVA (anti-CD36 vs LPS *p ≤ 0.05, LPS vs anti-CD36 + LPS *p ≤ 0.05).
    Figure Legend Snippet: Real-time bioluminescence imaging of theTLR2 signals after LPS challenge. ( a ) Schematic presentation of experimental protocol used for the treatment with anti-CD36 antibodies in P8-P9 mice. ( b – j ) Representative images of the bioluminescent signals recorded from the brains of living P10–P12 TLR2-luc-GFP mice treated with anti-CD36 antibody ( b – d ), LPS ( e – g ) or pre-treated with anti-CD36 antibody followed by systemic LPS injection ( h – j ). Note that a robust TLR2 induction 24 h post-LPS treatment is significantly reduced when the pups are pre-treated with anti-CD36. The scales on the right are the colour maps for source intensity. The scale ranges differ at individual ages. ( k ) Quantification of the in vivo bioluminescence data from P8–P12 (in photons per second, p/s). One way ANOVA (anti-CD36 vs LPS *p ≤ 0.05, LPS vs anti-CD36 + LPS *p ≤ 0.05).

    Techniques Used: Imaging, Injection, In Vivo

    Neonatal microglia demonstrate a reduced classical phenotype when treated with anti-CD36 antibody. ( a – v ) Immunostaining of neonatal brain sections with classical and alternative microglia phenotypic markers ( a – r ), with astrocyte marker GFAP ( s , t ) and IB4 ( u , v ). ( w ) Area of the cortical section analysed and quantification of CD68, MHC II, GFAP and IB4 expression ( x ). Microglial cells (Iba1 +) show increased expression of the classical activation markers CD86 ( a – f ) and MHCII ( g – l ) after systemic LPS injection (x). Their expression is significantly diminished when the pups are pre-treated with anti-CD36 antibody ( d – f and j – l ). Quantification of the signals in arbitrary units shows an overall decrease in expression of the classical markers when the pups are injected with anti-CD36 before the LPS treatment ( x ). Microglia in both the groups did not express the alternative microglial activation marker CD206 ( m – r ). No significant decrease was observed with the astrocytic marker GFAP in LPS and anti-CD36 + LPS treated pups ( s , t , x ). A non-significant decrease in the expression of IB4 is observed in the anti-CD36 + LPS pups when compared to the LPS treated pups ( u , v , x ). Scale bar is 100 µm. Unpaired t test with Welch's correction ***p ≤ 0.001; **p ≤ 0.01.
    Figure Legend Snippet: Neonatal microglia demonstrate a reduced classical phenotype when treated with anti-CD36 antibody. ( a – v ) Immunostaining of neonatal brain sections with classical and alternative microglia phenotypic markers ( a – r ), with astrocyte marker GFAP ( s , t ) and IB4 ( u , v ). ( w ) Area of the cortical section analysed and quantification of CD68, MHC II, GFAP and IB4 expression ( x ). Microglial cells (Iba1 +) show increased expression of the classical activation markers CD86 ( a – f ) and MHCII ( g – l ) after systemic LPS injection (x). Their expression is significantly diminished when the pups are pre-treated with anti-CD36 antibody ( d – f and j – l ). Quantification of the signals in arbitrary units shows an overall decrease in expression of the classical markers when the pups are injected with anti-CD36 before the LPS treatment ( x ). Microglia in both the groups did not express the alternative microglial activation marker CD206 ( m – r ). No significant decrease was observed with the astrocytic marker GFAP in LPS and anti-CD36 + LPS treated pups ( s , t , x ). A non-significant decrease in the expression of IB4 is observed in the anti-CD36 + LPS pups when compared to the LPS treated pups ( u , v , x ). Scale bar is 100 µm. Unpaired t test with Welch's correction ***p ≤ 0.001; **p ≤ 0.01.

    Techniques Used: Immunostaining, Marker, Expressing, Activation Assay, Injection

    Treatment with anti-CD36 antibody reduces expression of inflammatory mediators after LPS challenge. ( a – x ) Protein expression of 24 inflammatory cytokines reveals a significant reduction in cytokines ( a ) TNF-a, ( b ) IFN-g, ( c ) IL-1b, ( e ) IL-6, ( f ) IL-10, ( h ) IL-13, ( i ) IL-17, along with ( k ) GCSF, ( l ) GM-CSF, ( m ) MCP-1 and chemokines ( p ) CCL3, ( r ) CCL11 ( s ) CCL24, ( u ) CXCL1, ( v ) CXCL9 and ( x ) CXCL13 when the pups are treated with anti-CD36 before LPS. Unpaired t-test ***p ≤ 0.001; **p ≤ 0.01 and *p ≤ 0.05.
    Figure Legend Snippet: Treatment with anti-CD36 antibody reduces expression of inflammatory mediators after LPS challenge. ( a – x ) Protein expression of 24 inflammatory cytokines reveals a significant reduction in cytokines ( a ) TNF-a, ( b ) IFN-g, ( c ) IL-1b, ( e ) IL-6, ( f ) IL-10, ( h ) IL-13, ( i ) IL-17, along with ( k ) GCSF, ( l ) GM-CSF, ( m ) MCP-1 and chemokines ( p ) CCL3, ( r ) CCL11 ( s ) CCL24, ( u ) CXCL1, ( v ) CXCL9 and ( x ) CXCL13 when the pups are treated with anti-CD36 before LPS. Unpaired t-test ***p ≤ 0.001; **p ≤ 0.01 and *p ≤ 0.05.

    Techniques Used: Expressing

    Blocking CD36 significantly alters TLR-2 and TLR-3 signalling. ( a ) Western blot of whole brain protein lysates from the control (saline), anti-CD36, LPS and anti-CD36 + LPS injected pups. ( b ) Iba1, ( c ) TLR2, ( d ) TLR3, ( e ) IRF7, ( f ) phosrpho-P65 expression levels were quantified in different conditions. GAPDH was used as loading control A significant increase in the levels of all the tested proteins is observed after LPS injection. Treating the pups with anti-CD36 before LPS injections considerably reduces their expression to the level as observed in the control pups. ( g ) Western blot of total protein lysates from the control, anti-CD36, LPS and anti-CD36 + LPS injected mice. ( h ) TLR4, ( i ) IRF3, ( j ) iNOS expression levels were quantified in above-described conditions. GAPDH is used as loading control. A significant increase in the levels of all the proteins tested is observed after LPS injection when compared to control and anti-CD36 treated mice. Of note, LPS-mediated increase in expression of TLR4/IRF3 is maintained in the anti-CD36 + LPS treated group. The entire data was presented as mean ± SEM and statistical significance between the groups was achieved using one-way ANOVA with Tukey’s multiple comparison test (ctl vs LPS, ctl vs anti-CD36, LPS vs anti-CD36 + LPS) and depicted as ****p ≤ 0.0001; ***p ≤ 0.001; **p ≤ 0.01 and *p ≤ 0.05.
    Figure Legend Snippet: Blocking CD36 significantly alters TLR-2 and TLR-3 signalling. ( a ) Western blot of whole brain protein lysates from the control (saline), anti-CD36, LPS and anti-CD36 + LPS injected pups. ( b ) Iba1, ( c ) TLR2, ( d ) TLR3, ( e ) IRF7, ( f ) phosrpho-P65 expression levels were quantified in different conditions. GAPDH was used as loading control A significant increase in the levels of all the tested proteins is observed after LPS injection. Treating the pups with anti-CD36 before LPS injections considerably reduces their expression to the level as observed in the control pups. ( g ) Western blot of total protein lysates from the control, anti-CD36, LPS and anti-CD36 + LPS injected mice. ( h ) TLR4, ( i ) IRF3, ( j ) iNOS expression levels were quantified in above-described conditions. GAPDH is used as loading control. A significant increase in the levels of all the proteins tested is observed after LPS injection when compared to control and anti-CD36 treated mice. Of note, LPS-mediated increase in expression of TLR4/IRF3 is maintained in the anti-CD36 + LPS treated group. The entire data was presented as mean ± SEM and statistical significance between the groups was achieved using one-way ANOVA with Tukey’s multiple comparison test (ctl vs LPS, ctl vs anti-CD36, LPS vs anti-CD36 + LPS) and depicted as ****p ≤ 0.0001; ***p ≤ 0.001; **p ≤ 0.01 and *p ≤ 0.05.

    Techniques Used: Blocking Assay, Western Blot, Control, Saline, Injection, Expressing, Comparison

    Blocking CD36 in human immature microglia affects the TLR3, TLR2-IRF7 but not TLR4/IRF-3 pathway. ( a ) Western blot of total protein lysates of HMC3 cells treated with anti-CD36 antibody, followed by LPS treatment after 24 h. Expression levels of ( b ) Iba-1, ( c ) TLR2, ( d ) TLR 3 along with ( e ) IRF 7, ( f ) p-P65, ( g ) TLR 4, ( h ) IRF-3, ( i ) iNOS were analysed and quantified. GAPDH was used as loading control. LPS treatment increases expression levels of all measured proteins while pre-treatment withanti-CD36 antibody prevented increase in their expression levels. Expressions of ( g ) TLR 4 and ( h ) IRF-3 ( i ) were not affected by anti-CD36 antibody pre-treatment.. Entire data in the figure was presented as mean ± SEM and statistical significance between the groups was achieved using one-way ANOVA with Tukey multiple comparison test and depicted as ****p ≤ 0.0001; ***p ≤ 0.001; **p ≤ 0.01 and *p ≤ 0.05.
    Figure Legend Snippet: Blocking CD36 in human immature microglia affects the TLR3, TLR2-IRF7 but not TLR4/IRF-3 pathway. ( a ) Western blot of total protein lysates of HMC3 cells treated with anti-CD36 antibody, followed by LPS treatment after 24 h. Expression levels of ( b ) Iba-1, ( c ) TLR2, ( d ) TLR 3 along with ( e ) IRF 7, ( f ) p-P65, ( g ) TLR 4, ( h ) IRF-3, ( i ) iNOS were analysed and quantified. GAPDH was used as loading control. LPS treatment increases expression levels of all measured proteins while pre-treatment withanti-CD36 antibody prevented increase in their expression levels. Expressions of ( g ) TLR 4 and ( h ) IRF-3 ( i ) were not affected by anti-CD36 antibody pre-treatment.. Entire data in the figure was presented as mean ± SEM and statistical significance between the groups was achieved using one-way ANOVA with Tukey multiple comparison test and depicted as ****p ≤ 0.0001; ***p ≤ 0.001; **p ≤ 0.01 and *p ≤ 0.05.

    Techniques Used: Blocking Assay, Western Blot, Expressing, Control, Comparison

    CD36 mediated-effects on TLR signalling pathways in neonatal brain and immature human microglia. A diagram showing the mechanism of the scavenger receptor CD36-TLR mediated signalling in neonatal mouse brain as well as human microglia. ( a ) schematic representation of the methodology used. Neonatal mice and HMC3 cells were treated with LPS or anti-CD36 + LPS. ( b ) Upon activation by various ligands, the TLR2-CD36 mediated MyD88 dependent pathway activates transcription of various inflammatory cytokines. Activated endosomal TLR3 activates IRF3, which promotes transcription of the genes related to type 1 Interferons. Interestingly, IRF3 is also activated by TLR4, through the TRAM-TRIFF complex mediated cascade. ( c ) Blocking CD36 with the antibody prior to the LPS stimulation affects the TLR2 and TLR3 mediated signalling while the TLR4-IRF3 pathway continues to contribute to inflammation in both neonatal mouse as well as in human microglial cells. The schematic was created with BioRender.com.
    Figure Legend Snippet: CD36 mediated-effects on TLR signalling pathways in neonatal brain and immature human microglia. A diagram showing the mechanism of the scavenger receptor CD36-TLR mediated signalling in neonatal mouse brain as well as human microglia. ( a ) schematic representation of the methodology used. Neonatal mice and HMC3 cells were treated with LPS or anti-CD36 + LPS. ( b ) Upon activation by various ligands, the TLR2-CD36 mediated MyD88 dependent pathway activates transcription of various inflammatory cytokines. Activated endosomal TLR3 activates IRF3, which promotes transcription of the genes related to type 1 Interferons. Interestingly, IRF3 is also activated by TLR4, through the TRAM-TRIFF complex mediated cascade. ( c ) Blocking CD36 with the antibody prior to the LPS stimulation affects the TLR2 and TLR3 mediated signalling while the TLR4-IRF3 pathway continues to contribute to inflammation in both neonatal mouse as well as in human microglial cells. The schematic was created with BioRender.com.

    Techniques Used: Activation Assay, Blocking Assay



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    cd36 receptor blocking antibody  (Biophotonic Solutions Inc)
    90
    Biophotonic Solutions Inc cd36 receptor blocking antibody
    Real-time bioluminescence imaging of theTLR2 signals after LPS challenge. ( a ) Schematic presentation of experimental protocol used for the treatment with <t>anti-CD36</t> antibodies in P8-P9 mice. ( b – j ) Representative images of the bioluminescent signals recorded from the brains of living P10–P12 TLR2-luc-GFP mice treated with anti-CD36 antibody ( b – d ), LPS ( e – g ) or pre-treated with anti-CD36 antibody followed by systemic LPS injection ( h – j ). Note that a robust TLR2 induction 24 h post-LPS treatment is significantly reduced when the pups are pre-treated with anti-CD36. The scales on the right are the colour maps for source intensity. The scale ranges differ at individual ages. ( k ) Quantification of the in vivo bioluminescence data from P8–P12 (in photons per second, p/s). One way ANOVA (anti-CD36 vs LPS *p ≤ 0.05, LPS vs anti-CD36 + LPS *p ≤ 0.05).
    Cd36 Receptor Blocking Antibody, supplied by Biophotonic Solutions Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cd36+receptor+blocking+antibody/pmc09911392-41-4-11?v=Biophotonic+Solutions+Inc
    Average 90 stars, based on 1 article reviews
    cd36 receptor blocking antibody - by Bioz Stars, 2026-08
    90/100 stars
    		  Buy from Supplier

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    Real-time bioluminescence imaging of theTLR2 signals after LPS challenge. ( a ) Schematic presentation of experimental protocol used for the treatment with anti-CD36 antibodies in P8-P9 mice. ( b – j ) Representative images of the bioluminescent signals recorded from the brains of living P10–P12 TLR2-luc-GFP mice treated with anti-CD36 antibody ( b – d ), LPS ( e – g ) or pre-treated with anti-CD36 antibody followed by systemic LPS injection ( h – j ). Note that a robust TLR2 induction 24 h post-LPS treatment is significantly reduced when the pups are pre-treated with anti-CD36. The scales on the right are the colour maps for source intensity. The scale ranges differ at individual ages. ( k ) Quantification of the in vivo bioluminescence data from P8–P12 (in photons per second, p/s). One way ANOVA (anti-CD36 vs LPS *p ≤ 0.05, LPS vs anti-CD36 + LPS *p ≤ 0.05).

    Journal: Scientific Reports

    Article Title: CD36 neutralisation blunts TLR2-IRF7 but not IRF3 pathway in neonatal mouse brain and immature human microglia following innate immune challenge

    doi: 10.1038/s41598-023-29423-0

    Figure Lengend Snippet: Real-time bioluminescence imaging of theTLR2 signals after LPS challenge. ( a ) Schematic presentation of experimental protocol used for the treatment with anti-CD36 antibodies in P8-P9 mice. ( b – j ) Representative images of the bioluminescent signals recorded from the brains of living P10–P12 TLR2-luc-GFP mice treated with anti-CD36 antibody ( b – d ), LPS ( e – g ) or pre-treated with anti-CD36 antibody followed by systemic LPS injection ( h – j ). Note that a robust TLR2 induction 24 h post-LPS treatment is significantly reduced when the pups are pre-treated with anti-CD36. The scales on the right are the colour maps for source intensity. The scale ranges differ at individual ages. ( k ) Quantification of the in vivo bioluminescence data from P8–P12 (in photons per second, p/s). One way ANOVA (anti-CD36 vs LPS *p ≤ 0.05, LPS vs anti-CD36 + LPS *p ≤ 0.05).

    Article Snippet: By using a specific CD36 receptor blocking antibody in conjunction with biophotonic/bioluminescence imaging in the live TLR2-luc GFP mice, here we show that systemic delivery of an anti-CD36 antibody completely blunts TLR2 induction following LPS-mediated innate immune challenge in P9 brain.

    Techniques: Imaging, Injection, In Vivo

    Neonatal microglia demonstrate a reduced classical phenotype when treated with anti-CD36 antibody. ( a – v ) Immunostaining of neonatal brain sections with classical and alternative microglia phenotypic markers ( a – r ), with astrocyte marker GFAP ( s , t ) and IB4 ( u , v ). ( w ) Area of the cortical section analysed and quantification of CD68, MHC II, GFAP and IB4 expression ( x ). Microglial cells (Iba1 +) show increased expression of the classical activation markers CD86 ( a – f ) and MHCII ( g – l ) after systemic LPS injection (x). Their expression is significantly diminished when the pups are pre-treated with anti-CD36 antibody ( d – f and j – l ). Quantification of the signals in arbitrary units shows an overall decrease in expression of the classical markers when the pups are injected with anti-CD36 before the LPS treatment ( x ). Microglia in both the groups did not express the alternative microglial activation marker CD206 ( m – r ). No significant decrease was observed with the astrocytic marker GFAP in LPS and anti-CD36 + LPS treated pups ( s , t , x ). A non-significant decrease in the expression of IB4 is observed in the anti-CD36 + LPS pups when compared to the LPS treated pups ( u , v , x ). Scale bar is 100 µm. Unpaired t test with Welch's correction ***p ≤ 0.001; **p ≤ 0.01.

    Journal: Scientific Reports

    Article Title: CD36 neutralisation blunts TLR2-IRF7 but not IRF3 pathway in neonatal mouse brain and immature human microglia following innate immune challenge

    doi: 10.1038/s41598-023-29423-0

    Figure Lengend Snippet: Neonatal microglia demonstrate a reduced classical phenotype when treated with anti-CD36 antibody. ( a – v ) Immunostaining of neonatal brain sections with classical and alternative microglia phenotypic markers ( a – r ), with astrocyte marker GFAP ( s , t ) and IB4 ( u , v ). ( w ) Area of the cortical section analysed and quantification of CD68, MHC II, GFAP and IB4 expression ( x ). Microglial cells (Iba1 +) show increased expression of the classical activation markers CD86 ( a – f ) and MHCII ( g – l ) after systemic LPS injection (x). Their expression is significantly diminished when the pups are pre-treated with anti-CD36 antibody ( d – f and j – l ). Quantification of the signals in arbitrary units shows an overall decrease in expression of the classical markers when the pups are injected with anti-CD36 before the LPS treatment ( x ). Microglia in both the groups did not express the alternative microglial activation marker CD206 ( m – r ). No significant decrease was observed with the astrocytic marker GFAP in LPS and anti-CD36 + LPS treated pups ( s , t , x ). A non-significant decrease in the expression of IB4 is observed in the anti-CD36 + LPS pups when compared to the LPS treated pups ( u , v , x ). Scale bar is 100 µm. Unpaired t test with Welch's correction ***p ≤ 0.001; **p ≤ 0.01.

    Article Snippet: By using a specific CD36 receptor blocking antibody in conjunction with biophotonic/bioluminescence imaging in the live TLR2-luc GFP mice, here we show that systemic delivery of an anti-CD36 antibody completely blunts TLR2 induction following LPS-mediated innate immune challenge in P9 brain.

    Techniques: Immunostaining, Marker, Expressing, Activation Assay, Injection

    Treatment with anti-CD36 antibody reduces expression of inflammatory mediators after LPS challenge. ( a – x ) Protein expression of 24 inflammatory cytokines reveals a significant reduction in cytokines ( a ) TNF-a, ( b ) IFN-g, ( c ) IL-1b, ( e ) IL-6, ( f ) IL-10, ( h ) IL-13, ( i ) IL-17, along with ( k ) GCSF, ( l ) GM-CSF, ( m ) MCP-1 and chemokines ( p ) CCL3, ( r ) CCL11 ( s ) CCL24, ( u ) CXCL1, ( v ) CXCL9 and ( x ) CXCL13 when the pups are treated with anti-CD36 before LPS. Unpaired t-test ***p ≤ 0.001; **p ≤ 0.01 and *p ≤ 0.05.

    Journal: Scientific Reports

    Article Title: CD36 neutralisation blunts TLR2-IRF7 but not IRF3 pathway in neonatal mouse brain and immature human microglia following innate immune challenge

    doi: 10.1038/s41598-023-29423-0

    Figure Lengend Snippet: Treatment with anti-CD36 antibody reduces expression of inflammatory mediators after LPS challenge. ( a – x ) Protein expression of 24 inflammatory cytokines reveals a significant reduction in cytokines ( a ) TNF-a, ( b ) IFN-g, ( c ) IL-1b, ( e ) IL-6, ( f ) IL-10, ( h ) IL-13, ( i ) IL-17, along with ( k ) GCSF, ( l ) GM-CSF, ( m ) MCP-1 and chemokines ( p ) CCL3, ( r ) CCL11 ( s ) CCL24, ( u ) CXCL1, ( v ) CXCL9 and ( x ) CXCL13 when the pups are treated with anti-CD36 before LPS. Unpaired t-test ***p ≤ 0.001; **p ≤ 0.01 and *p ≤ 0.05.

    Article Snippet: By using a specific CD36 receptor blocking antibody in conjunction with biophotonic/bioluminescence imaging in the live TLR2-luc GFP mice, here we show that systemic delivery of an anti-CD36 antibody completely blunts TLR2 induction following LPS-mediated innate immune challenge in P9 brain.

    Techniques: Expressing

    Blocking CD36 significantly alters TLR-2 and TLR-3 signalling. ( a ) Western blot of whole brain protein lysates from the control (saline), anti-CD36, LPS and anti-CD36 + LPS injected pups. ( b ) Iba1, ( c ) TLR2, ( d ) TLR3, ( e ) IRF7, ( f ) phosrpho-P65 expression levels were quantified in different conditions. GAPDH was used as loading control A significant increase in the levels of all the tested proteins is observed after LPS injection. Treating the pups with anti-CD36 before LPS injections considerably reduces their expression to the level as observed in the control pups. ( g ) Western blot of total protein lysates from the control, anti-CD36, LPS and anti-CD36 + LPS injected mice. ( h ) TLR4, ( i ) IRF3, ( j ) iNOS expression levels were quantified in above-described conditions. GAPDH is used as loading control. A significant increase in the levels of all the proteins tested is observed after LPS injection when compared to control and anti-CD36 treated mice. Of note, LPS-mediated increase in expression of TLR4/IRF3 is maintained in the anti-CD36 + LPS treated group. The entire data was presented as mean ± SEM and statistical significance between the groups was achieved using one-way ANOVA with Tukey’s multiple comparison test (ctl vs LPS, ctl vs anti-CD36, LPS vs anti-CD36 + LPS) and depicted as ****p ≤ 0.0001; ***p ≤ 0.001; **p ≤ 0.01 and *p ≤ 0.05.

    Journal: Scientific Reports

    Article Title: CD36 neutralisation blunts TLR2-IRF7 but not IRF3 pathway in neonatal mouse brain and immature human microglia following innate immune challenge

    doi: 10.1038/s41598-023-29423-0

    Figure Lengend Snippet: Blocking CD36 significantly alters TLR-2 and TLR-3 signalling. ( a ) Western blot of whole brain protein lysates from the control (saline), anti-CD36, LPS and anti-CD36 + LPS injected pups. ( b ) Iba1, ( c ) TLR2, ( d ) TLR3, ( e ) IRF7, ( f ) phosrpho-P65 expression levels were quantified in different conditions. GAPDH was used as loading control A significant increase in the levels of all the tested proteins is observed after LPS injection. Treating the pups with anti-CD36 before LPS injections considerably reduces their expression to the level as observed in the control pups. ( g ) Western blot of total protein lysates from the control, anti-CD36, LPS and anti-CD36 + LPS injected mice. ( h ) TLR4, ( i ) IRF3, ( j ) iNOS expression levels were quantified in above-described conditions. GAPDH is used as loading control. A significant increase in the levels of all the proteins tested is observed after LPS injection when compared to control and anti-CD36 treated mice. Of note, LPS-mediated increase in expression of TLR4/IRF3 is maintained in the anti-CD36 + LPS treated group. The entire data was presented as mean ± SEM and statistical significance between the groups was achieved using one-way ANOVA with Tukey’s multiple comparison test (ctl vs LPS, ctl vs anti-CD36, LPS vs anti-CD36 + LPS) and depicted as ****p ≤ 0.0001; ***p ≤ 0.001; **p ≤ 0.01 and *p ≤ 0.05.

    Article Snippet: By using a specific CD36 receptor blocking antibody in conjunction with biophotonic/bioluminescence imaging in the live TLR2-luc GFP mice, here we show that systemic delivery of an anti-CD36 antibody completely blunts TLR2 induction following LPS-mediated innate immune challenge in P9 brain.

    Techniques: Blocking Assay, Western Blot, Control, Saline, Injection, Expressing, Comparison

    Blocking CD36 in human immature microglia affects the TLR3, TLR2-IRF7 but not TLR4/IRF-3 pathway. ( a ) Western blot of total protein lysates of HMC3 cells treated with anti-CD36 antibody, followed by LPS treatment after 24 h. Expression levels of ( b ) Iba-1, ( c ) TLR2, ( d ) TLR 3 along with ( e ) IRF 7, ( f ) p-P65, ( g ) TLR 4, ( h ) IRF-3, ( i ) iNOS were analysed and quantified. GAPDH was used as loading control. LPS treatment increases expression levels of all measured proteins while pre-treatment withanti-CD36 antibody prevented increase in their expression levels. Expressions of ( g ) TLR 4 and ( h ) IRF-3 ( i ) were not affected by anti-CD36 antibody pre-treatment.. Entire data in the figure was presented as mean ± SEM and statistical significance between the groups was achieved using one-way ANOVA with Tukey multiple comparison test and depicted as ****p ≤ 0.0001; ***p ≤ 0.001; **p ≤ 0.01 and *p ≤ 0.05.

    Journal: Scientific Reports

    Article Title: CD36 neutralisation blunts TLR2-IRF7 but not IRF3 pathway in neonatal mouse brain and immature human microglia following innate immune challenge

    doi: 10.1038/s41598-023-29423-0

    Figure Lengend Snippet: Blocking CD36 in human immature microglia affects the TLR3, TLR2-IRF7 but not TLR4/IRF-3 pathway. ( a ) Western blot of total protein lysates of HMC3 cells treated with anti-CD36 antibody, followed by LPS treatment after 24 h. Expression levels of ( b ) Iba-1, ( c ) TLR2, ( d ) TLR 3 along with ( e ) IRF 7, ( f ) p-P65, ( g ) TLR 4, ( h ) IRF-3, ( i ) iNOS were analysed and quantified. GAPDH was used as loading control. LPS treatment increases expression levels of all measured proteins while pre-treatment withanti-CD36 antibody prevented increase in their expression levels. Expressions of ( g ) TLR 4 and ( h ) IRF-3 ( i ) were not affected by anti-CD36 antibody pre-treatment.. Entire data in the figure was presented as mean ± SEM and statistical significance between the groups was achieved using one-way ANOVA with Tukey multiple comparison test and depicted as ****p ≤ 0.0001; ***p ≤ 0.001; **p ≤ 0.01 and *p ≤ 0.05.

    Article Snippet: By using a specific CD36 receptor blocking antibody in conjunction with biophotonic/bioluminescence imaging in the live TLR2-luc GFP mice, here we show that systemic delivery of an anti-CD36 antibody completely blunts TLR2 induction following LPS-mediated innate immune challenge in P9 brain.

    Techniques: Blocking Assay, Western Blot, Expressing, Control, Comparison

    CD36 mediated-effects on TLR signalling pathways in neonatal brain and immature human microglia. A diagram showing the mechanism of the scavenger receptor CD36-TLR mediated signalling in neonatal mouse brain as well as human microglia. ( a ) schematic representation of the methodology used. Neonatal mice and HMC3 cells were treated with LPS or anti-CD36 + LPS. ( b ) Upon activation by various ligands, the TLR2-CD36 mediated MyD88 dependent pathway activates transcription of various inflammatory cytokines. Activated endosomal TLR3 activates IRF3, which promotes transcription of the genes related to type 1 Interferons. Interestingly, IRF3 is also activated by TLR4, through the TRAM-TRIFF complex mediated cascade. ( c ) Blocking CD36 with the antibody prior to the LPS stimulation affects the TLR2 and TLR3 mediated signalling while the TLR4-IRF3 pathway continues to contribute to inflammation in both neonatal mouse as well as in human microglial cells. The schematic was created with BioRender.com.

    Journal: Scientific Reports

    Article Title: CD36 neutralisation blunts TLR2-IRF7 but not IRF3 pathway in neonatal mouse brain and immature human microglia following innate immune challenge

    doi: 10.1038/s41598-023-29423-0

    Figure Lengend Snippet: CD36 mediated-effects on TLR signalling pathways in neonatal brain and immature human microglia. A diagram showing the mechanism of the scavenger receptor CD36-TLR mediated signalling in neonatal mouse brain as well as human microglia. ( a ) schematic representation of the methodology used. Neonatal mice and HMC3 cells were treated with LPS or anti-CD36 + LPS. ( b ) Upon activation by various ligands, the TLR2-CD36 mediated MyD88 dependent pathway activates transcription of various inflammatory cytokines. Activated endosomal TLR3 activates IRF3, which promotes transcription of the genes related to type 1 Interferons. Interestingly, IRF3 is also activated by TLR4, through the TRAM-TRIFF complex mediated cascade. ( c ) Blocking CD36 with the antibody prior to the LPS stimulation affects the TLR2 and TLR3 mediated signalling while the TLR4-IRF3 pathway continues to contribute to inflammation in both neonatal mouse as well as in human microglial cells. The schematic was created with BioRender.com.

    Article Snippet: By using a specific CD36 receptor blocking antibody in conjunction with biophotonic/bioluminescence imaging in the live TLR2-luc GFP mice, here we show that systemic delivery of an anti-CD36 antibody completely blunts TLR2 induction following LPS-mediated innate immune challenge in P9 brain.

    Techniques: Activation Assay, Blocking Assay