Toll-like receptor 5 knock-out mice exhibit a specific low level of anxiety

2021 ◽  
Author(s):  
A.M. Hamieh ◽  
G. Mallaret ◽  
M. Meleine ◽  
A. Lashermes ◽  
S. Roumeau ◽  
...  
Keyword(s):  
Toll Like Receptor ◽  
Knock Out ◽  
Low Level ◽  
Knock Out Mice ◽  
Toll Like Receptor 5

Cardiotoxicity of anthracycline: Novel approach through down regulation of TLR-3 via TRAF/MAPK signaling pathway

2015 ◽  
Vol 3 (2) ◽  
pp. 423-432
Author(s):  
Robyn Wonder ◽  
Steliana Penzkofer ◽  
Evelyn G Hazen
Keyword(s):  
Mapk Signaling ◽  
Lv Function ◽  
Toll Like Receptor ◽  
Cardiac Damage ◽  
Male Adult ◽  
Knock Out ◽  
Monocyte Chemoattractant Protein 1 ◽  
Novel Approach ◽  
Heart Injury ◽  
Knock Out Mice

Cardiotoxicity is one of the most important complications doxorubicin (DOX) and its pathomechanisms are not completely elucidated. We hypothesize that signaling via toll-like receptor (TLR)-3, a receptor that is activated upon binding of double-stranded nucleotides, might play a crucial role in the pathogenesis of cardiac-toxicity following DOX treatment. Male adult C57BL6 wild-type mice and TLR-3 knock-out (-/-) mice were subjected to 20 mg/kg; administered intraperitoneally. TLR-3 down-stream signaling was activated in WT mice lead to strong pro-inflammatory response with significant monocyte cells invasion. In contrast, this effect was attenuated in TLR-3-/- mice. Moreover, the TLR-3 activation resulted in cardiac damage that was associated with significantly reduced LV function and increased monocyte chemoattractant protein-1 (MCP)-1 expression in WT mice. This finding was confirmed by increased MAPK and TRIF protein expression in WT mice. This study confirmed that the absence of TLR-3 is associated with lower heart injury and maintained LV function. Thus, we conclude that TLR-3 seems to participate in the pathogenesis of cardiotoxicity of DOX.

Cardiotoxicity of anthracycline: Novel approach through down regulation of TLR-3 via TRAF/MAPK signaling pathway

2015 ◽  
Vol 2 (3) ◽  
pp. 423-432
Keyword(s):  
Mapk Signaling ◽  
Lv Function ◽  
Toll Like Receptor ◽  
Cardiac Damage ◽  
Male Adult ◽  
Knock Out ◽  
Monocyte Chemoattractant Protein 1 ◽  
Novel Approach ◽  
Heart Injury ◽  
Knock Out Mice

Cardiotoxicity is one of the most important complications doxorubicin (DOX) and its pathomechanisms are not completely elucidated. We hypothesize that signaling via toll-like receptor (TLR)-3, a receptor that is activated upon binding of double-stranded nucleotides, might play a crucial role in the pathogenesis of cardiac-toxicity following DOX treatment. Male adult C57BL6 wild-type mice and TLR-3 knock-out (-/-) mice were subjected to 20 mg/kg; administered intraperitoneally. TLR-3 down-stream signaling was activated in WT mice lead to strong pro-inflammatory response with significant monocyte cells invasion. In contrast, this effect was attenuated in TLR-3-/- mice. Moreover, the TLR-3 activation resulted in cardiac damage that was associated with significantly reduced LV function and increased monocyte chemoattractant protein-1 (MCP)-1 expression in WT mice. This finding was confirmed by increased MAPK and TRIF protein expression in WT mice. This study confirmed that the absence of TLR-3 is associated with lower heart injury and maintained LV function. Thus, we conclude that TLR-3 seems to participate in the pathogenesis of cardiotoxicity of DOX.

Cardiotoxicity of anthracycline: Novel approach through down regulation of TLR-3 via TRAF/MAPK signaling pathway

2015 ◽  
Vol 2 (3) ◽  
pp. 423-432
Author(s):  
Robyn Wonder ◽  
Steliana Penzkofer ◽  
Evelyn G Hazen
Keyword(s):  
Mapk Signaling ◽  
Lv Function ◽  
Toll Like Receptor ◽  
Cardiac Damage ◽  
Male Adult ◽  
Knock Out ◽  
Monocyte Chemoattractant Protein 1 ◽  
Novel Approach ◽  
Heart Injury ◽  
Knock Out Mice

Cardiotoxicity is one of the most important complications doxorubicin (DOX) and its pathomechanisms are not completely elucidated. We hypothesize that signaling via toll-like receptor (TLR)-3, a receptor that is activated upon binding of double-stranded nucleotides, might play a crucial role in the pathogenesis of cardiac-toxicity following DOX treatment. Male adult C57BL6 wild-type mice and TLR-3 knock-out (-/-) mice were subjected to 20 mg/kg; administered intraperitoneally. TLR-3 down-stream signaling was activated in WT mice lead to strong pro-inflammatory response with significant monocyte cells invasion. In contrast, this effect was attenuated in TLR-3-/- mice. Moreover, the TLR-3 activation resulted in cardiac damage that was associated with significantly reduced LV function and increased monocyte chemoattractant protein-1 (MCP)-1 expression in WT mice. This finding was confirmed by increased MAPK and TRIF protein expression in WT mice. This study confirmed that the absence of TLR-3 is associated with lower heart injury and maintained LV function. Thus, we conclude that TLR-3 seems to participate in the pathogenesis of cardiotoxicity of DOX.

scholarly journals Toll-like receptor 5 as a novel receptor for fungal zymosan

2021 ◽  
Author(s):  
Stefanie Reuter ◽  
Kristina Herold ◽  
Jana Domroes ◽  
Ralf Mrowka
Keyword(s):  
Innate Immune ◽  
Microbial Pathogens ◽  
Toll Like Receptor ◽  
Knock Out ◽  
Activation Of Transcription ◽  
Host Defense Response ◽  
Toll Like Receptor 5 ◽  
Molecular Patterns ◽  
First Time ◽  
Luciferase Reporters

Microbial pathogens carry specific structural patterns which were termed pathogenassociated molecular patterns (PAMPs). Toll-like receptors (TLRs) as key elements for the recognition of microbial pathogens are necessary for the activation of innate immune pathways. TLRs are activated by binding PAMPs of bacteria, viruses and fungi and initiate a signaling pathway resulting in the activation of transcription factors which modulate the production of various proinflammatory cytokines. It is not fully clear in detail which microbial pattern is recognized by which TLR. Here we show for the first time that TLR5 is a strong receptor for the yeast particle zymosan. We have generated stable human cell lines with combinations of TLR2 and TLR5 knock in/knock out together with stable nuclear factor kappaB (NF-κB) luciferase reporters. We found that both receptors TLR5 and TLR2 lead to an independent activation of the NF-κB pathway when simulated with zymosan. Our results demonstrate that TLR5 is a receptor for the fungal particle zymosan in addition to bacterial fragments like flagellin. Distinct cytokine patterns might suggest that TLR5 is potentially important for the differentiation in the recognition of the specific type of the foreign microorganisms and in the specific host defense response.

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