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Int J Med Microbiol. 2017 Oct 27. pii: S1438-4221(17)30306-5. doi: 10.1016/j.ijmm.2017.10.004. [Epub ahead of print]

Innate sensing and cell-autonomous resistance pathways in Legionella pneumophila infection.

Author information

1
Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Augustenburger Platz 1, 13353 Berlin, Germany.
2
Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Augustenburger Platz 1, 13353 Berlin, Germany; German Center for Lung Research (DZL), Germany. Electronic address: bastian.opitz@charite.de.

Abstract

Legionella pneumophila is a facultative intracellular bacterium which can cause a severe pneumonia called Legionnaires' disease after inhalation of contaminated water droplets and replication in alveolar macrophages. The innate immune system is generally able to sense and -in most cases- control L. pneumophila infection. Comorbidities and genetic risk factors, however, can compromise the immune system and high infection doses might overwhelm its capacity, thereby enabling L. pneumophila to grow and disseminate inside the lung. The innate immune system mediates sensing of L. pneumophila by employing e.g. NOD-like receptors (NLRs), Toll-like receptors (TLRs), as well as the cGAS/STING pathway to stimulate death of infected macrophages as well as production of proinflammatory cytokines and interferons (IFNs). Control of pulmonary L. pneumophila infection is largely mediated by inflammasome-, TNFα- and IFN-dependent macrophage-intrinsic resistance mechanisms. This article summarizes the current knowledge of innate immune responses to L. pneumophila infection in general, and of macrophage-intrinsic defense mechanisms in particular.

KEYWORDS:

Cell-autonomous defense; Ifn; Innate immunity; Legionella pneumophila

PMID:
29097162
DOI:
10.1016/j.ijmm.2017.10.004

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