title: Bacteria tune interferon responses by playing with chromatin.
abstract: Bacterial infections, like their viral counterparts, trigger the onset of innate immune defense mechanisms through the release of cytokines, including interferons (IFNs). While type I and II IFN responses to bacteria have long been explored, type III IFN response remains poorly addressed. We have recently reported that the pathogen Listeria monocytogenes triggers the expression of type I and III IFN genes in epithelial cells, and is able to fine-tune downstream signaling at the chromatin level. This bacterium can negatively or positively modulate the expression of interferon-stimulated genes (ISGs) by manipulating the function of BAHD1, a component of a host chromatin-silencing complex. To this end, L. monocytogenes tightly controls the secretion of a BAHD1 inhibitory factor, LntA. Here, we further document the current knowledge about chromatin mechanisms modulating interferon responses during host-bacteria interplay, and discuss their physiological consequences.
authors.affiliation: Institut Pasteur, Unité des Interactions Bactéries-Cellules, Paris, France.
authors.forename: Alice
authors.initials: A
authors.lastname: Lebreton
authors.forename: Pascale
authors.initials: P
authors.lastname: Cossart
authors.forename: Hélène
authors.initials: H
authors.lastname: Bierne
mesh_terms: D000818:Animals; D002843:Chromatin / Q000235:genetics / Q000276:immunology*; D002868:Chromosomal Proteins, Non-Histone / Q000235:genetics / Q000276:immunology; D054884:Host-Pathogen Interactions; D006801:Humans; D007372:Interferons / Q000235:genetics / Q000276:immunology*; D008089:Listeria monocytogenes / Q000235:genetics / Q000502:physiology*; D008088:Listeriosis / Q000235:genetics / Q000276:immunology* / Q000382:microbiology*; D051379:Mice
chemical_list: D002843:Chromatin; D002868:Chromosomal Proteins, Non-Histone; D007372:Interferons