Project description:Innate memory is a key defence mechanism against infection, enhancing protective immunity and limiting unnecessary collateral tissue damage. Inflammation triggered by endogenous stimuli that signal cellular stress or tissue injury, must also be tightly controlled to balance robust response to intrinsic danger whilst avoiding catastrophic autoimmunity. Here, we assess the contribution of innate memory to this balance. The extracellular matrix protein tenascin-C, a damage-associated, toll-like receptor 4 (TLR4) agonist, reprograms monocyte response to subsequent threat, inducing concomitantly suppressed and enhanced responses to rechallenge. Comparative analysis of memory evoked by tenascin-C and the pathogenic TLR4 agonist, LPS, revealed both common and distinct gene expression signatures, effects that were controlled transcriptionally, These data highlight how intrinsic and extrinsic innate re-programming exerts control over dysregulated inflammatory networks driving either infectious or chronic ‘sterile’ inflammatory diseases.

2025-05-06 | GSE273837 | GEO

Gene Expression Regulation in Brain Underlying Innate Immune Memory

Project description:Gene Expression Regulation in Brain Underlying Innate Immune Memory

| PRJNA693876 | ENA

PAMPS and Innate Immune Memory

Project description:Exposure to pathogen-associated molecular patterns (PAMPs) induces an augmented, broad-spectrum antimicrobial response to subsequent infection, a phenomenon termed innate immune memory. This study examined the effects of treatment with β-glucan, a fungus-derived Dectin-1 ligand, and monophosphoryl lipid A (MPLA), a bacteria-derived TNS4 ligand, on innate immune memory with a focus on identifying common cellular and molecular pathways. Treatment with either PAMP prepared the innate immune system to respond more robustly to Pseudomonas aeruginosa infection in vivo by facilitating mobilization of innate leukocytes into blood, their recruitment to the site of infection, augmentation of microbial clearance and attenuation of cytokine production. Examination of macrophages ex vivo showed that metabolism, phagocytosis and respiratory burst were amplified by treatment with either agent, although MPLA more robustly augmented these activities and more effectively facilitated killing of bacteria. Both agents activated gene expression pathways in macrophages that control inflammation, antimicrobial functions and protein synthesis and suppressed pathways regulating cell division with MPLA more potently inducing global gene transcription. β-glucan treatment minimally modified macrophage differential gene expression in response to LPS challenge compared to control whereas MPLA attenuated the magnitude of the LPS-induced transcriptional response. These results show that b-glucan and MPLA similarly augment the innate response to infection in vivo. Yet, MPLA more potently induces alterations in macrophage metabolism, antimicrobial functions, gene transcription and the response to LPS.

2023-08-23 | GSE240614 | GEO

Galectin-7 reprograms skin carcinogenesis by fostering innate immune evasive programs

Project description:Galectin-7 reprograms skin carcinogenesis by fostering innate immune evasive programs

| PRJNA693872 | ENA

innate immune cell memory induced by endogenous and exogenous triggers

Project description:innate immune cell memory induced by endogenous and exogenous triggers

| PRJNA1143447 | ENA

Innate immune memory in the brain shapes neurological disease hallmarks

Project description:Innate immune memory in the brain shapes neurological disease hallmarks

| PRJNA324246 | ENA