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Increased inflammation and impaired resistance to Chlamydophila pneumoniae infection in Dusp1(-/-) mice: Critical role of IL-6.
J. Leukoc. Biol. 88, 579-587 (2010)
The MAPK phosphatase DUSP1 is an essential negative regulator of TLR-triggered innate immune activation. Here, we have investigated the impact of DUSP1 on inflammatory and antimicrobial host responses to the intracellular pathogen Chlamydophila pneumoniae. Following nasal infection, DUSP1-deficient mice mounted an enhanced pulmonary cytokine (IL-1beta, IL-6) and chemokine response (CCL3, CCL4, CXCL1, CXCL2), leading to increased leukocyte infiltration. Of interest, the increased inflammatory response, in the absence of DUSP1, was associated with higher bacterial numbers in the lungs, although the expression of IFN-gamma and critical antichlamydial effector molecules, such as iNOS, was intact. Blockade of IL-6 trans-signaling by injection of a soluble gp130-Fc fusion protein corrected the overshooting chemokine production as well as the increased chlamydial load in Dusp1(-/-) mice. Furthermore, IL-6 enhanced the replication of C. pneumoniae in embryonic fibroblasts in vitro. These data show that DUSP1 is required to achieve a balanced response to chlamydial infection and identify IL-6 as critical for amplifying inflammation and benefiting chlamydial growth through direct effects on infected cells.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
host-pathogen interactions; signal transduction
Language
english
Publication Year
2010
HGF-reported in Year
2010
ISSN (print) / ISBN
0741-5400
e-ISSN
1938-3673
Journal
Journal of Leukocyte Biology
Quellenangaben
Volume: 88,
Issue: 3,
Pages: 579-587
Publisher
FASEB
Reviewing status
Peer reviewed
Institute(s)
Institute of Pathology (PATH)
POF-Topic(s)
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Research field(s)
Enabling and Novel Technologies
PSP Element(s)
G-500300-001
PubMed ID
20483921
Scopus ID
77957168184
Erfassungsdatum
2010-12-31