Bacteria tune interferon responses by playing with chromatin.

Area of Science:

• Immunology
• Microbiology
• Epigenetics

Background:

• Bacterial infections trigger innate immune responses, including cytokine release like interferons (IFNs).
• Type I and II IFN responses are well-studied, but type III IFN responses to bacteria are less understood.
• Epithelial cells are crucial in host defense against bacterial pathogens.

Purpose of the Study:

• To investigate the role of type III interferons (IFNs) in host defense against bacterial infections.
• To elucidate the mechanisms by which Listeria monocytogenes modulates interferon-stimulated gene (ISG) expression.
• To explore the involvement of chromatin remodeling and the BAHD1 complex in bacterial pathogenesis.

Main Methods:

• Analysis of type I and III IFN gene expression in epithelial cells upon Listeria monocytogenes infection.
• Investigation of chromatin modifications associated with interferon-stimulated genes (ISGs).
• Study of the bacterial factor LntA and its role in inhibiting the host chromatin-silencing complex BAHD1.

Main Results:

• Listeria monocytogenes induces both type I and type III IFN gene expression in epithelial cells.
• The bacterium modulates ISG expression by manipulating the BAHD1 chromatin-silencing complex.
• L. monocytogenes secretes LntA to inhibit BAHD1, thereby controlling ISG expression.

Conclusions:

• Type III IFNs play a significant role in the epithelial response to bacterial infections.
• Bacterial pathogens can exploit host chromatin mechanisms, like BAHD1, to evade or manipulate immune responses.
• Understanding these host-pathogen interactions at the chromatin level is crucial for developing new therapeutic strategies.