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Synergistic hepatoprotective effect of the TLR5 agonist CBLB502 and its downstream effector IL-22

ABSTRACT: Synergistic hepatoprotective effect of the TLR5 agonist CBLB502 and its downstream effector IL-22

PROVIDER: PRJNA673242 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12939246_1.fastq.gz	Fastqsanger.gz
	SRR12939246_2.fastq.gz	Fastqsanger.gz
	SRR12939247_1.fastq.gz	Fastqsanger.gz
	SRR12939247_2.fastq.gz	Fastqsanger.gz
	SRR12939248_1.fastq.gz	Fastqsanger.gz

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Synergistic hepatoprotective effect of the TLR5 agonist CBLB502 and its downstream effector IL-22

Project description:We have shown that CBLB502 (CBLB) display hepatoprotective activities, and triggers a strong IL-22 release. To understand the hepatoprotection, we describe the response of isolated adult mouse hepatocyte to IL-22, CBLB, or IL-22 + CBLB exposure.

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Protection of TLR5 agonist, CBLB502, against cisplatin treated mouse liver and kidney

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Synergistic effect of the TLR5 agonist CBLB502 and its downstream effector IL-22 against liver injury.

Project description:The toll-like receptor 5 (TLR5) agonist, CBLB502/Entolimod, is a peptide derived from bacterial flagellin and has been shown to protect against radiation-induced tissue damage in animal models. Here we investigated the protective mechanism of CBLB502 in the liver using models of ischemia-reperfusion injury and concanavalin A (ConA) induced immuno-hepatitis. We report that pretreatment of mice with CBLB502 provoked a concomitant activation of NF-κB and STAT3 signaling in the liver and reduced hepatic damage in both models. To understand the underlying mechanism, we screened for cytokines in the serum of CBLB502 treated animals and detected high levels of IL-22. There was no transcriptional upregulation of IL-22 in the liver, rather it was found in extrahepatic tissues, mainly the colon, mesenteric lymph nodes (MLN), and spleen. RNA-seq analysis on isolated hepatocytes demonstrated that the concomitant activation of NF-κB signaling by CBLB502 and STAT3 signaling by IL-22 produced a synergistic cytoprotective transcriptional signature. In IL-22 knockout mice, the loss of IL-22 resulted in a decrease of hepatic STAT3 activation, a reduction in the cytoprotective signature, and a loss of hepatoprotection following ischemia-reperfusion-induced liver injury. Taken together, these findings suggest that CBLB502 protects the liver by increasing hepatocyte resistance to acute liver injury through the cooperation of TLR5-NF-κB and IL-22-STAT3 signaling pathways.

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Protection of TLR5 agonist, CBLB502, against cisplatin treated mouse liver and kidney

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