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THP-1 cell lines treated with or without BTC and TLR2/4 ligands, and their subsequent gene expression

ABSTRACT: THP-1 cell lines treated with or without BTC and TLR2/4 ligands, and their subsequent gene expression

PROVIDER: PRJNA889389 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21861800.fastq.gz	Fastqsanger.gz
	SRR21861779.fastq.gz	Fastqsanger.gz
	SRR21861780.fastq.gz	Fastqsanger.gz
	SRR21861781.fastq.gz	Fastqsanger.gz
	SRR21861782.fastq.gz	Fastqsanger.gz

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THP-1 cell lines treated with or without BTC and TLR2/4 ligands, and their subsequent gene expression

Project description:THP-1 cells treated with or without BTC and TLR2/4 ligands

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Beyond Pattern Recognition: TLR2 Promotes Chemotaxis, Cell Adhesion and Migration in THP-1 Cells

Project description:The interaction between monocytes and endothelial cells in inflammation is central to chemoattraction, adhesion, and transendothelial migration. Key players such as selectins and their ligands, integrins and other adhesion molecules and their function in these processes are well studied. Toll-like receptor 2 (TLR2), expressed on monocytes, is critical for sensing invading pathogens and initiating a rapid and effective immune response. However, the extended role of TLR2 in monocyte adhesion and migration has only been partially elucidated. To address this question, we performed several functional cell-based assays using monocyte-like wild type (WT), TLR2-knock-out (KO) and, TLR2-knock-in (KI) THP-1 cells. We found that TLR2 promotes faster and stronger adhesion of monocytes to the endothelium and a more intense endothelial barrier disruption after endothelial activation. In addition, we performed quantitative mass-spectrometry, STRING protein analysis, and RT-qPCR, which revealed the association of TLR2 with specific integrins, but also uncovered novel proteins affected by TLR2. In conclusion, we could show that unstimulated TLR2 affects cell adhesion, endothelial barrier disruption, migration, and actin polymerization.

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Whole blood gene expression after stimulation with TLR2 ligands (chitin oligomers, Pam2, Pam3) and the TLR4-ligand LPS

Project description:Chitin is the second most abundant polysaccharide in nature and a biomolecule intimately linked to fungal infection and allergic asthma, conditions that affect millions of patients worldwide. Chitin is known to stimulate multiple mammalian immune cells, but the precise molecular sensing mechanism has not been elucidated, hampering strategies to specifically target chitin-mediated pathologies. The study associated with this microarray dataset uses defined chitin oligomers to identify six chitin subunits as the smallest immunologically active chitin motif and the innate immune receptor TLR2 as the molecular chitin sensor on human and murine immune cells, in vitro and in vivo. The goal of this microarray dataset was to elucidate transcriptional differences of human whole blood cells when responding to chitin, to other TLR2 ligands (Pam2, Pam3), and furthermore to the TLR4 ligand LPS. All four stimulants are compared to each other and to the unstimulated whole blood samples as a reference. We conclude that chitin oligomers elicitd overlapping yet distinct signaling outcomes compared to canonical TLR2 ligands.

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Bacterial TLR2/6 Ligands Block Ciliogenesis, Derepress Hedgehog Signaling, and Expand the Neocortex

Project description:Bacterial TLR2/6 Ligands Block Ciliogenesis, Derepress Hedgehog Signaling, and Expand the Neocortex

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Project description:Inflammation can both repress and promote tumor progression depending on the type, frequency, and combination with different therapeutic modalities. In acute myeloid leukemia (AML) generation of effector cells of the innate immune system are attenuated, suggesting that innate immune function has a critical role in leukemogenesis. Using a panel of ligands directed at the Toll-like family of pattern recognition receptors (TLRs) to induce acute inflammation in models of high-risk AML, we uncover that TLR2 ligands exert unique anti-leukemia effects distinct from other TLRs, through cell-type specific autonomous and non-autonomous mechanisms. TLR2 signaling causes non-specific inflammatory-mediated AML cell death, leukemia stem cell (LSC) reprogramming with impaired self-renewal, bi-lineage myeloid maturation, and prolonged survival. Subsequent cytokine signaling both promotes and antagonizes these AML-intrinsic effects, at least in part through G-CSF released from cells in the bone marrow microenvironment. Importantly, TLR2 is the most abundant TLR expressed in human AML regardless of ELN or mutation status, suggesting a key role in human disease. Together, these data indicate functional interplay of innate immune signaling between AML cells and the microenvironment during acute inflammation directly impacts leukemia progression.

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