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Garlicki, G.

Publications and source records attributed to Garlicki, G..

2 recordsLinked to original sources

Lifestyle-mediated shifts in the gut microbiome and host genetics modulate gene expression in intestinal organoids

Industrialization-associated shifts in the gut microbiome have been linked to disease, but the mechanisms by which microbial communities influence host gene regulation remain poorly understood. We developed a live microbiome-colonic organoid (colonoid) co-culture system to investigate genotype-dependent host responses to gut microbial community variation. Colonoid 2D monolayers from healthy donors were co-cultured with live gut microbial communities from individuals living urban or rural lifestyles, followed by RNA-sequencing. Urban and rural microbiomes elicited largely shared transcriptional responses, however they induced distinct host genetic effects on gene expression. We identified 511 host genes with microbiome-dependent allele-specific expression (ASE) which were involved in epithelial architecture, cell-matrix interactions and structural integrity. Notably, 149 host genes had distinct allelic effects between Urban and Rural microbiomes (urban-rural condition specific ASE or cASE), revealing genotype-dependent host responses to lifestyle-associated microbiomes. Urban-rural cASE was associated with microbial community composition, predominantly involving Prevotella and Bacteroides species. Targeted Prevotella copri spike-in recapitulated Prevotella-associated allelic effects at specific loci, including one in the IBD-associated autophagy gene, ATG4B. Together, these findings establish an experimental framework to investigate genotype-by-microbiome interactions, and demonstrate that lifestyle-mediated shifts in the microbiome modify host cis-regulatory genetic effects on gene expression.

genomics↗

Psychological stress and social support are associated with opposing single-cell pro-inflammatory gene regulatory mechanisms in adults

Psychological stress is linked to elevated markers of chronic inflammation, whereas social support is associated with lower levels; yet, the molecular mechanisms mediating these effects are poorly understood. We investigated gene regulatory variation in peripheral blood mononuclear cells (PBMCs) from 165 self-reported African American adults (aged 50-89 years) using single-cell RNA sequencing (scRNA-seq) and single-cell chromatin accessibility (scATAC-seq). Self-reported psychological stress and social support were associated with differential expression of 1,956 and 1,296 genes, respectively (10% FDR), primarily in CD4+ T cells and monocytes. Interferon signaling genes showed high expression in individuals with high psychological stress and low expression in those with high social support; this pattern mirrored gene expression in individuals with elevated circulating inflammatory markers (IFN-{gamma}, TNF-, IL-6). Genome-wide transcription factor (TF) motif analysis identified stress- and social support-associated changes in motif activity for 70 and 116 TFs, respectively, with 87 motifs enriched near differentially expressed genes. In CD4+ T cells, high psychological stress corresponded to increased IRF and STAT TF motif activity (interferon pathway), while social support was associated with reduced activity and expression in these pathways. We used an immune challenge paradigm (i.e., LPS stimulation), which confirmed the biological pathways of these gene regulatory effects. Our results demonstrate that psychological stress and social support modulate immune gene regulation at the single-cell level, revealing mechanistic links between psychosocial factors and inflammation, and suggesting that social support may promote immunological health.

genomics↗