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RNA-seq of human monocytic cell line (THP-1) treated with compound #42 (2D216), LPS, #42(2D216)/LPS, or vehicle controls

ABSTRACT: To explore the effects of compound #42 on RNA transcription of THP-1 cells, we performed RNA-seq analysis.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Homo sapiens

SUBMITTER: Tomoko Hayashi

PROVIDER: E-MTAB-10222 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Small Molecule Calcium Channel Activator Potentiates Adjuvant Activity.

Saito Tetsuya T Shukla Nikunj M NM Sato-Kaneko Fumi F Sako Yukiya Y Hosoya Tadashi T Yao Shiyin S Lao Fitzgerald S FS Messer Karen K Pu Minya M Chan Michael M Chu Paul J PJ Cottam Howard B HB Hayashi Tomoko T Carson Dennis A DA Corr Maripat M

ACS chemical biology 20220105 1

There remains an unmet need for reliable fully synthetic adjuvants that increase lasting protective immune responses from vaccines. We previously reported a high-throughput screening for small molecules that extended nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB) activation after a Toll-like receptor 4 (TLR4) ligand, lipopolysaccharide (LPS), stimulation using a human myeloid reporter cell line. We identified compounds with a conserved aminothiazole scaffold including <b> ...[more]

PMID: 34985883

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RNA-seq of human monocytic cell line (THP-1) treated with compound 81 or vehicle controls

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RNA-seq of human monocytic cell line (THP-1) treated with compound #1 or vehicle controls

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RNA-seq of human monocytic cell line (THP-1) treated with compound #42, LPS, #42/LPS, or vehicle controls

Project description:RNA-seq of human monocytic cell line (THP-1) treated with compound #42, LPS, #42/LPS, or vehicle controls

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Amyloid Beta Peptide (Aβ1-42) Reverses the Cholinergic Control of Monocytic IL-1β Release.

Project description:Amyloid-β peptide (Aβ1-42), the cleavage product of the evolutionary highly conserved amyloid precursor protein, presumably plays a pathogenic role in Alzheimer's disease. Aβ1-42 can induce the secretion of the pro-inflammatory cytokine intereukin-1β (IL-1β) in immune cells within and out of the nervous system. Known interaction partners of Aβ1-42 are α7 nicotinic acetylcholine receptors (nAChRs). The physiological functions of Aβ1-42 are, however, not fully understood. Recently, we identified a cholinergic mechanism that controls monocytic release of IL-1β by canonical and non-canonical agonists of nAChRs containing subunits α7, α9, and/or α10. Here, we tested the hypothesis that Aβ1-42 modulates this inhibitory cholinergic mechanism. Lipopolysaccharide-primed monocytic U937 cells and human mononuclear leukocytes were stimulated with the P2X7 receptor agonist 2'(3')-O-(4-benzoylbenzoyl)adenosine-5'-triphosphate triethylammonium salt (BzATP) in the presence or absence of nAChR agonists and Aβ1-42. IL-1β concentrations were measured in the supernatant. Aβ1-42 dose-dependently (IC50 = 2.54 µM) reversed the inhibitory effect of canonical and non-canonical nicotinic agonists on BzATP-mediated IL-1β-release by monocytic cells, whereas reverse Aβ42-1 was ineffective. In conclusion, we discovered a novel pro-inflammatory Aβ1-42 function that enables monocytic IL-1β release in the presence of nAChR agonists. These findings provide evidence for a novel physiological function of Aβ1-42 in the context of sterile systemic inflammation.

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Nitric oxide exposure induces production of Rpf-dependent differentially culturable mycobacteria

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