<it>Legionella pneumophila </it>induces human beta Defensin-3 in pulmonary cells

Respiratory Research. 2010;11(1):93 DOI 10.1186/1465-9921-11-93

 

Journal Homepage

Journal Title: Respiratory Research

ISSN: 1465-9921 (Print); 1465-993X (Online)

Publisher: BMC

LCC Subject Category: Medicine: Internal medicine: Specialties of internal medicine: Diseases of the respiratory system

Country of publisher: United Kingdom

Language of fulltext: English

Full-text formats available: PDF, HTML

 

AUTHORS

Hippenstiel Stefan
Heuner Klaus
Flieger Antje
Opitz Bastian
Schmeck Bernd
Lang Friederike
Vardarova Kremena
Scharf Stefanie
Suttorp Norbert
N'Guessan Philippe D

EDITORIAL INFORMATION

Blind peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 17 weeks

 

Abstract | Full Text

<p>Abstract</p> <p>Background</p> <p><it>Legionella pneumophila </it>is an important causative agent of severe pneumonia in humans. Human alveolar epithelium and macrophages are effective barriers for inhaled microorganisms and actively participate in the initiation of innate host defense. The beta defensin-3 (hBD-3), an antimicrobial peptide is an important component of the innate immune response of the human lung. Therefore we hypothesize that hBD-3 might be important for immune defense towards <it>L. pneumophila</it>.</p> <p>Methods</p> <p>We investigated the effects of <it>L. pneumophila </it>and different TLR agonists on pulmonary cells in regard to hBD-3 expression by ELISA. Furthermore, siRNA-mediated inhibition of TLRs as well as chemical inhibition of potential downstream signaling molecules was used for functional analysis.</p> <p>Results</p> <p><it>L. pneumophila </it>induced release of hBD-3 in pulmonary epithelium and alveolar macrophages. A similar response was observed when epithelial cells were treated with different TLR agonists. Inhibition of TLR2, TLR5, and TLR9 expression led to a decreased hBD-3 expression. Furthermore expression of hBD-3 was mediated through a JNK dependent activation of AP-1 (c-Jun) but appeared to be independent of NF-κB. Additionally, we demonstrate that hBD-3 elicited a strong antimicrobial effect on <it>L. pneumophila </it>replication.</p> <p>Conclusions</p> <p>Taken together, human pulmonary cells produce hBD-3 upon <it>L. pneumophila </it>infection via a TLR-JNK-AP-1-dependent pathway which may contribute to an efficient innate immune defense.</p>