Department of Microbiology Papers

Document Type

Journal Article

Date of this Version


Publication Source

Cellular Microbiology





Start Page


Last Page





Defense mechanisms against intracellular bacterial pathogens are incompletely understood. Our study characterizes a type I IFN-dependent cell-autonomous defense pathway directed against Legionella pneumophila, an intracellular model organism and frequent cause of pneumonia. We show that macrophages infected with L. pneumophila produced IFNβ in a STING- and IRF3- dependent manner. Paracrine type I IFNs stimulated up-regulation of IFN-stimulated genes and a cell-autonomous defense pathway acting on replicating and non-replicating Legionella within their specialized vacuole. Our infection experiments in mice lacking receptors for type I and/or II IFNs show that type I IFNs contribute to expression of IFN-stimulated genes and to bacterial clearance as well as resistance in L. pneumophila pneumonia in addition to type II IFN. Overall, our study shows that paracrine type I IFNs mediate defense against L. pneumophila, and demonstrates a protective role of type I IFNs in in vivo infections with intracellular bacteria.

Copyright/Permission Statement

This is the peer reviewed version of the following article: Lippman, J., Müller, H.C., Naujoks, J., Tabeling, C., Shin, S., Witzenrath, M., Hellwig, K., Kirschning, C.J., Taylor, G.A., Barchet, W., Bauer, S., Suttorp, N., Roy, C.R., and Opitz, B.: Dissection of a type I interferon pathway in controlling bacterial intracellular infection in mice. Cellular Microbiology 13(11): 1668-1682, 2011., which has been published in final form at This article may be used for non-commercial purposes in accordance With Wiley Terms and Conditions for self-archiving.


At the time of publication, author Sunny Shin was affiliated with Yale University School of Medicine. Currently, she is a faculty member at the Department of Microbiology at the University of Pennsylvania.



Date Posted: 09 May 2017

This document has been peer reviewed.