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Chromatin accessibility dynamics of Chlamydia-infected epithelial cells.

ABSTRACT: Chlamydia are Gram-negative, obligate intracellular bacterial pathogens responsible for a broad spectrum of human and animal diseases. In humans, Chlamydia trachomatis is the most prevalent bacterial sexually transmitted infection worldwide and is the causative agent of trachoma (infectious blindness) in disadvantaged populations. Over the course of its developmental cycle, Chlamydia extensively remodels its intracellular niche and parasitises the host cell for nutrients, with substantial resulting changes to the host cell transcriptome and proteome. However, little information is available on the impact of chlamydial infection on the host cell epigenome and global gene regulation. Regions of open eukaryotic chromatin correspond to nucleosome-depleted regions, which in turn are associated with regulatory functions and transcription factor binding. We applied formaldehyde-assisted isolation of regulatory elements enrichment followed by sequencing (FAIRE-Seq) to generate temporal chromatin maps of C. trachomatis-infected human epithelial cells in vitro over the chlamydial developmental cycle. We detected both conserved and distinct temporal changes to genome-wide chromatin accessibility associated with C. trachomatis infection. The observed differentially accessible chromatin regions include temporally-enriched sets of transcription factors, which may help shape the host cell response to infection. These regions and motifs were linked to genomic features and genes associated with immune responses, re-direction of host cell nutrients, intracellular signalling, cell-cell adhesion, extracellular matrix, metabolism and apoptosis. This work provides another perspective to the complex response to chlamydial infection, and will inform further studies of transcriptional regulation and the epigenome in Chlamydia-infected human cells and tissues.

SUBMITTER: Hayward RJ

PROVIDER: S-EPMC7590614 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Chromatin accessibility dynamics of Chlamydia-infected epithelial cells.

Hayward Regan J RJ Marsh James W JW Humphrys Michael S MS Huston Wilhelmina M WM Myers Garry S A GSA

Epigenetics & chromatin 20201027 1

Chlamydia are Gram-negative, obligate intracellular bacterial pathogens responsible for a broad spectrum of human and animal diseases. In humans, Chlamydia trachomatis is the most prevalent bacterial sexually transmitted infection worldwide and is the causative agent of trachoma (infectious blindness) in disadvantaged populations. Over the course of its developmental cycle, Chlamydia extensively remodels its intracellular niche and parasitises the host cell for nutrients, with substantial result ...[more]

PMID: 33109274

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Project description:Pasteurella multocida can cause goat hemorrhagic sepsis and endemic pneumonia. Respiratory epithelial cells are the first line of defense in the lungs during P. multocida infection. These cells act as a mechanical barrier and activate immune response to protect against invading pathogenic microorganisms. Upon infection, P. multocida adheres to the cells and causes changes in cell morphology and transcriptome. ATAC-seq was conducted to determine the changes in the chromatin open region of P. multocida-infected goat bronchial epithelial cells based on transcriptional regulation. A total of 13,079 and 28,722 peaks were identified in the control (CK) and treatment (T) groups (P. multocida infection group), respectively. The peaks significantly increased after P. multocida infection. The specific peaks for the CK and T groups were annotated to 545 and 6632 genes, respectively. KEGG pathway enrichment analysis revealed that the specific peak-related genes in the T group were enriched in immune reaction-related pathways, such as Fc gamma R-mediated phagocytosis, MAPK signaling pathway, bacterial invasion of epithelial cells, endocytosis, and autophagy pathways. Other cellular component pathways were also enriched, including the regulation of actin cytoskeleton, adherent junction, tight junction, and focal adhesion. The differential peaks between the two groups were subsequently analyzed. Compared to those in the CK group, 863 and 11 peaks were upregulated and downregulated, respectively, after the P. multocida infection. Fifty-six known transcription factor motifs were revealed in upregulated peaks in the P. multocida-infected group. By integrating ATAC-seq and RNA-seq, some candidate genes (SETBP1, RASGEF1B, CREB5, IRF5, TNF, CD70) that might be involved in the goat bronchial epithelial cell immune reaction to P. multocida infection were identified. Overall, P. multocida infection changed the structure of the cell and caused chromatin open regions to be upregulated. In addition, P. multocida infection actively mobilized the host immune response with the inflammatory phenotype. The findings provide valuable information for understanding the regulatory mechanisms of P. multocida-infected goat bronchial epithelial cells.

Dataset Information

Chromatin accessibility dynamics of Chlamydia-infected epithelial cells.

Publications

Chromatin accessibility dynamics of Chlamydia-infected epithelial cells.

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