TREM-1 amplifies inflammation and is a crucial mediator of septic shock

Axel Bouchon, Fabio Facchetti, Markus A. Weigand and Marco Colonna ()
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Axel Bouchon: Basel Institute for Immunology
Fabio Facchetti: Institute of Pathology, University of Brescia, Spedali Civili 1
Markus A. Weigand: Clinic of Anaesthesiology, University of Heidelberg and Tumor Immunology Program, German Cancer Research Institute, (DKFZ), INF 110,280
Marco Colonna: Basel Institute for Immunology

Nature, 2001, vol. 410, issue 6832, 1103-1107

Abstract: Abstract Host innate responses to bacterial infections are primarily mediated by neutrophils and monocytes/macrophages1,2. These cells express pattern recognition receptors (PRRs) that bind conserved molecular structures shared by groups of microorganisms3,4. Stimulation of PRR signalling pathways initiates secretion of proinflammatory mediators3,4, which promote the elimination of infectious agents and the induction of tissue repair. Excessive inflammation owing to bacterial infections can lead to tissue damage and septic shock5,6,7,8,9. Here we show that inflammatory responses to microbial products are amplified by a pathway mediated by triggering receptor expressed on myeloid cells (TREM)-1. TREM-1 is an activating receptor expressed at high levels on neutrophils and monocytes that infiltrate human tissues infected with bacteria. Furthermore, it is upregulated on peritoneal neutrophils of patients with microbial sepsis and mice with experimental lipopolysaccaride (LPS)-induced shock. Notably, blockade of TREM-1 protects mice against LPS-induced shock, as well as microbial sepsis caused by live Escherichia coli or caecal ligation and puncture. These results demonstrate a critical function of TREM-1 in acute inflammatory responses to bacteria and implicate TREM-1 as a potential therapeutic target for septic shock.

Date: 2001
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DOI: 10.1038/35074114

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