Document Detail

TREM-1 activation alters the dynamics of pulmonary IRAK-M expression in vivo and improves host defense during pneumococcal pneumonia.
MedLine Citation:
PMID:  19596984     Owner:  NLM     Status:  MEDLINE    
Triggering receptor expressed on myeloid cells-1 (TREM-1) is an amplifier of TLR-mediated inflammation during bacterial infections. Thus far, TREM-1 is primarily associated with unwanted signs of overwhelming inflammation, rendering it an attractive target for conditions such as sepsis. Respiratory tract infections are the leading cause of sepsis, but the biological role of TREM-1 therein is poorly understood. To determine the function of TREM-1 in pneumococcal pneumonia, we first established TREM-1 up-regulation in infected lungs and human plasma together with augmented alveolar macrophage responsiveness toward Streptococcus pneumoniae. Mice treated with an agonistic TREM-1 Ab and infected with S. pneumoniae exhibited an enhanced early induction of the inflammatory response that was indirectly associated with lower levels of negative regulators of TLR signaling in lung tissue in vivo. Later in infection, TREM-1 engagement altered S. pneumoniae-induced IRAK-M (IL-1R-associated kinase-M) kinetics so as to promote the resolution of pneumonia and remarkably led to an accelerated elimination of bacteria and consequently improved survival. These data show that TREM-1 exerts a protective role in the innate immune response to a common bacterial infection and suggest that caution should be exerted in modulating TREM-1 activity during certain clinically relevant bacterial infections.
Heimo Lagler; Omar Sharif; Isabella Haslinger; Ulrich Matt; Karin Stich; Tanja Furtner; Bianca Doninger; Katharina Schmid; Rainer Gattringer; Alex F de Vos; Sylvia Knapp
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-07-13
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  183     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-07-21     Completed Date:  2009-08-06     Revised Date:  2012-06-27    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2027-36     Citation Subset:  AIM; IM    
Department of Medicine I, Division of Infectious Diseases and Tropical Medicine, Medical University Vienna, Vienna, Austria.
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MeSH Terms
Gene Expression Regulation
Immunity, Innate*
Interleukin-1 Receptor-Associated Kinases / genetics*
Lung / metabolism,  pathology
Macrophages, Alveolar / immunology
Membrane Glycoproteins / immunology*
Pneumonia, Pneumococcal / immunology*
Receptors, Immunologic / immunology*
Streptococcus pneumoniae
Reg. No./Substance:
0/Membrane Glycoproteins; 0/Receptors, Immunologic; 0/TREM1 protein, human; 0/TREM1 protein, mouse; EC Receptor-Associated Kinases; EC protein, mouse

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