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MAdCAM-1 targeting strategy can prevent colitic cancer carcinogenesis and progression via suppression of immune cell infiltration and inflammatory signals

ABSTRACT: MAdCAM-1 targeting strategy can prevent colitic cancer carcinogenesis and progression via suppression of immune cell infiltration and inflammatory signals

PROVIDER: PRJNA991527 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25158732.fastq.gz	Fastqsanger.gz
	SRR25158733.fastq.gz	Fastqsanger.gz
	SRR25158734.fastq.gz	Fastqsanger.gz
	SRR25158735.fastq.gz	Fastqsanger.gz

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MAdCAM-1 targeting strategy can prevent colitic cancer carcinogenesis and progression via suppression of immune cell infiltration and inflammatory signals

Project description:Chronic inflammation caused by infiltrating immune cells can promote colitis-associated dysplasia/colitic cancer in ulcerative colitis (UC) by activating inflammatory cytokine signaling through the IL-6/p-STAT3 and TNFα/NF-κB pathways. Mucosal addressin cell adhesion molecule-1 (MAdCAM-1) expressed on high endothelial venules promotes the migration of immune cells from the bloodstream to the gut via interaction with α4β7 integrin expressed on the immune cells. MAdCAM-1, has therefore drawn interest as a novel therapeutic target for treating active UC. However, the role of MAdCAM-1-positive endothelial cells in immune cell infiltration in dysplasia/colitic cancers remains unclear. We evaluated the expression of MAdCAM-1, CD31, and immune cell markers (CD8, CD68, CD163, and FOXP3) in samples surgically resected from 11 UC patients with dysplasia/colitic cancer and 17 patients with sporadic colorectal cancer (SCRC), using immunohistochemical staining. We used an azoxymethane/dextran sodium sulfate mouse model (AOM/DSS mouse) to evaluate whether dysplasia/colitic cancer could be suppressed with an anti-MAdCAM-1 blocking antibody by preventing immune cell infiltration. The number of MAdCAM-1-positive vessels and infiltrating CD8+, CD68+, and CD163+ immune cells was significantly higher in dysplasia/colitic cancer than in normal, SCRC, and UC mucosa. In AOM/DSS mice, the anti-MAdCAM-1 antibody reduced the number, mean diameter, depth of tumors, Ki67 positivity, number of CD8+, CD68+, and CD163+ immune cells, and the IL-6/p-STAT3 and TNF-α/NF-κB signaling. Our results indicate that targeting MAdCAM-1 is a promising strategy for controlling not only UC severity, but also carcinogenesis and tumor progression by regulating inflammation/immune cell infiltration in patients with UC.

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Project description:Fecal samples collected on day 5 from randomly selected colitic SD rats were analyzed for gut microbiota by sequencing the V4 region of the 16S rRNA gene. The orally administered Dex-P-laden NPA2 coacervate (Dex-P/NPA2) significantly restores the diversity of gut microbiota compared with colitic SD rats in the Dex-P/PBS group and the untreated colitic rats (Control).

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